Pylori Culture Research Articles

Gastric bypass surgery does not increase susceptibility to Helicobacter pylori infection in the stomach of rat or mouse

Gastric bypass is a clinical option for obesity surgery. An increased susceptibility to Helicobacter pylori infection in the bypassed stomach has been speculated. The aim of the present study was to examine the susceptibility of the bypassed stomach to H. pylori infection in rats and mice. Adult Sprague-Dawley and Wistar rats and NMRI mice were subjected to either gastric bypass or laparotomy only as control. The animals were inoculated with the CagA- and VacA- positive H. pylori strain 67/21 (not mouse-adapted) in the first experiment and with 9 additional isolates in the second, by injection into the bypassed stomach or the control stomach during surgery. The stomach of each animal was collected for H. pylori culture 2-3 weeks later. While all the rats were H. pylori negative, 54% of gastric bypassed mice and 75% of controls were positive (P = 0.4). We conclude that susceptibility to H. pylori infection in the stomach is not increased by gastric bypass surgery.

Biofilm formation and modulation of luxS and rpoD expression by Helicobacter pylori

Bacteria often choose a sessile biofilm lifestyle as a strategy to overcome environmental stress. In this study, we describe biofilm formation by Helicobacter pylori on a polystyrene surface, evaluating the viability and the morphological dynamics of bacterial cells during multicellular aggregate development. Moreover, we investigate expression of the luxS and rpoD genes, which are involved in biofilm formation.Two clinically susceptible and resistant strains of H. pylori were analyzed, as well as H. pylori ATCC 43629 for reference. The dominant form of expression, clustered bacterial cells arranged in an abundant matrix, was recorded after 2 days of incubation without shaking. Coccoid (spherical) cells with a “wrinkled” aspect presented the prevalent morphology (59.26%) among cells in the biofilm structure as observed by scanning electron microscopy. In aged H. pylori cultures, death occurred in single cells or cells grouped into microcolonies in which degenerated bacteria were localized inside the aggregates. The expression of luxS and rpoD genes among the sessile bacterial population reached a maximum after 2 days, with a significant reduction at subsequent time-points. No differences in gene expression and biofilm formation were recorded in the three evaluated strains.The morphological fickleness expressed in the life cycle by H. pylori strains emphasizes the bacterium's ability to overcome environmental stress, balancing its spread both outside and inside the host.

Posttreatment 13C-urea breath test is predictive of antimicrobial resistance to H. pylori after failed therapy

We tested whether a 13C-urea breath test can predict antimicrobial resistance of Helicobacter pylori (H. pylori). Seventy patients who had failed triple eradication therapy and 108 untreated H. pylori-infected patients were given a 13C-urea breath test, endoscopy for culture of H. pylori, and assessment of clarithromycin resistance. The patients who had failed triple therapy then received 1 week of quadruple therapy to eradicate residual H. pylori. The posttreatment value of the 13C-urea breath test expressed as excessive delta13CO2 per ml (ECR) was higher in patients with residual H. pylori with clarithromycin resistance than in those without (23.8 vs 10.6; P<.0001). With a cutoff of ECR >or< or =15, the 13C-urea breath test was 88.6% sensitive and 88.9% specific in predicting clarithromycin resistance of residual H. pylori. The H. pylori eradication rate of the rescue regimen was higher for patients with a posttreatment ECR of the 13C-urea breath test < or =15 than for those with a value >15 (93.8% vs 73.3%; P<.05). In contrast, in treatment-naive H. pylori-infected patients, the pretreatment value of the 13C-urea breath test did not differ between patients infected with clarithromycin-resistant or-sensitive isolates (P>.05). The posttreatment value of the 13C-urea breath test is predictive of clarithromycin resistance in residual H. pylori after failed triple therapy and predicts efficacy of the rescue regimen. The value of the noninvasive test is promising for primary care physicians who need to select a rescue regimen without invasive H. pylori culture.

Topographical localisation of cagA positive and cagA negative Helicobacter pylori strains in the gastric mucosa; an in situ hybridisation study

Background: The cagA gene is a marker for the presence of the cag pathogenicity island, and the presence of cagA positive strains of Helicobacter pylori can identify individuals with a...

The influence of endoscopic procedures upon the contamination of Helicobacter pylori cultures

Among the various diagnostic methods for the detection of Helicobacter pylori infection, histological examination and microbiological processing of gastric biopsy samples are assumed to be the gold standard techniques. Since H. pylori culture can be affected by the presence of non-H. pylori bacteria, we evaluated the efficacy of endoscope disinfection and the influence of endoscopic procedures on culture contamination. The procedures used during the first two routine endoscopies were evaluated during 28 consecutive days. Endoscopy room, forceps and endoscopic channel were analyzed before and after the beginning of normal procedures. After disinfection, a biopsy simulation was performed to verify the gastric bacteria. Endoscope disinfection removed all organisms from forceps and endoscopic channel with 100% efficacy. The most frequent non-H. pylori bacteria detected were Streptococcus bovis, Enterobacter hormaechei, and Staphylococcus aureus. The sensibility of the H. pylori culture was affected by the presence of non-H. pylori bacteria. The risk of transmission of microorganisms was not detectable when sterilized biopsy forceps and stringent disinfection standards were employed. Whilst S. bovis and E. hormaechei may be common in gastric microbial flora, the presence of P. aeruginosa and S. aureus indicated that the manipulation of biopsies could be responsible for culture contamination with these bacteria.

Primary Helicobacter pylori resistance to metronidazole and clarithromycin in the Finnish population.

To systematically determine Helicobacter pylori primary antimicrobial resistance in Finland and the associated demographic and clinical features. A total of 342 adult patients referred for gastroscopy at 23 centres in different parts of Finland and positive for the rapid biopsy urease test were recruited. Clinical and demographic data were collected via a structured questionnaire. Patients with positive H. pylori culture and successful antibiotic sensitivity determination by the E-test method (n = 292) were included in the present analysis. The study population consisted of 134 men and 158 women, mean age 56 years (95% CI, 55-58 years). Resistance to metronidazole was 38% (110 of 292) and to clarithromycin 2% (seven of 292). Resistance to metronidazole was higher in women than in men (48% vs. 25%, P < 0.001). Previous use of antibiotics for gynaecological infections predicted metronidazole resistance (P = 0.01), and previous use of antibiotics for respiratory (P = 0.02) and dental infections (P = 0.02) the clarithromycin resistance. We observed no major geographical variations in metronidazole resistance. The primary metronidazole resistance of H. pylori was 38% and was common in women previously treated for gynaecological infections. Primary clarithromycin resistance was uncommon (2%) and may associate with previous dental and respiratory infections.

Gastroesophageal Reflux Disease and Helicobacter pylori Infection in Neurologically Impaired Children: Inter‐relations and Therapeutic Implications

ABSTRACTBackgroundThe aim of this retrospective study was to assess the relationship between Helicobacter pylori infection and gastroesophageal reflux disease in a high‐risk population of children.MethodsForty‐three neurologically impaired pediatric patients with H. pylori had upper gastrointestinal endoscopy between 1990 and 2000. Infection was confirmed by positive H. pylori culture or by identification of organisms in gastric biopsy specimens (fundus, n = 2; antrum, n = 3). Reflux esophagitis was diagnosed by ulceration of the esophageal mucosa at endoscopy. Four to 6 weeks after the completion of antibiotic treatment of H. pylori, a second endoscopy was performed and the gross appearance of the esophagus was recorded.ResultsAt the first endoscopy, esophagitis was noted in 14 of 43 patients. After treatment, H. pylori infection was eradicated in all 14 patients with esophagitis but in only 19 of 29 (66%) of those with normal esophagus (P = 0.01). Esophagitis was still present in 4 of 14 (29%) patients who had esophagitis at the first endoscopy. Persistent esophagitis was only related to the presence of esophagitis before treatment (P = 0.02). In 29 patients with a normal esophagus at the first endoscopy, only one case of esophagitis was observed after H. pylori eradication.ConclusionThe data suggest that treatment of H. pylori infection should be considered in children with concomitant GERD, and such treatment is unlikely to either induce or exacerbate peptic esophagitis.

Gastroesophageal reflux disease and Helicobacter pylori infection in neurologically impaired children: inter-relations and therapeutic implications.

The aim of this retrospective study was to assess the relationship between Helicobacter pylori infection and gastroesophageal reflux disease in a high-risk population of children. Forty-three neurologically impaired pediatric patients with H. pylori had upper gastrointestinal endoscopy between 1990 and 2000. Infection was confirmed by positive H. pylori culture or by identification of organisms in gastric biopsy specimens (fundus, n = 2; antrum, n = 3). Reflux esophagitis was diagnosed by ulceration of the esophageal mucosa at endoscopy. Four to 6 weeks after the completion of antibiotic treatment of H. pylori, a second endoscopy was performed and the gross appearance of the esophagus was recorded. At the first endoscopy, esophagitis was noted in 14 of 43 patients. After treatment, H. pylori infection was eradicated in all 14 patients with esophagitis but in only 19 of 29 (66%) of those with normal esophagus (P = 0.01). Esophagitis was still present in 4 of 14 (29%) patients who had esophagitis at the first endoscopy. Persistent esophagitis was only related to the presence of esophagitis before treatment (P = 0.02). In 29 patients with a normal esophagus at the first endoscopy, only one case of esophagitis was observed after H. pylori eradication. The data suggest that treatment of H. pylori infection should be considered in children with concomitant GERD, and such treatment is unlikely to either induce or exacerbate peptic esophagitis.

Growth of Helicobacter pylori in medium supplemented with cyanobacterial extract.

Solid and liquid media supplemented only with a cyanobacterial extract (CE) and free of fetal calf serum (FCS), blood, and its derivatives support the growth of Helicobacter pylori. A total of 11 strains of H. pylori isolated from gastric biopsy samples were successfully subcultured in Mueller-Hinton agar supplemented with 0.4% CE. When this medium was used for primary isolation of H. pylori, a low isolation rate (30%) was observed because of the abundant growth of contaminants. The growth kinetics of eight isolates and H. pylori reference strain NCTC 11638 in Mueller-Hinton broth (MHB) supplemented with 0.7% CE were estimated by use of growth parameters, and the results were compared with those obtained with MHB-5% FCS. For four strains the cellular concentrations obtained with CE were statistically higher (P < 0.05) than those obtained with FCS, and in some cases these values were similar to the highest values reported in the literature. Depending on the strain, the specific growth rates obtained with CE were similar to or increased compared with those obtained with FCS. The replacement of FCS by CE in H. pylori cultures would facilitate the retrieval of cultures with high cellular densities as a source of cellular and extracellular proteins free of serum. Also, CE has advantages over conventional supplements, such as easier conservation and compliance with the pressing tendency at present to avoid the use of products derived from animals.

Ultrastructural observation of Helicobacter pylori in glucose-supplemented culture media.

Helicobacter pylori in the human gut can be divided morphologically into spiral and coccoid forms. The spiral form is known to change into the coccoid form in culture in vitro. The ultrastructural changes and culturability of H. pylori were studied in medium supplemented with different concentrations of glucose. H. pylori ATCC 43504(T) was cultured in liquid medium containing 10 % heat-inactivated horse serum supplemented with glucose (at 0, 10, 100, 300 and 500 mM) for 7 days. Bacterial ultrastructure and culturability were examined daily. With extended time in culture, the spiral forms had transformed into coccoid forms in all media. The coccoid forms could be further divided into two types, A and B, by electron microscopy. The type A coccoid form had an irregular surface with few flagella and indistinct cytoplasmic membrane. The type B coccoid form had a better-maintained integral membrane structure and was the dominant form in 300 mM glucose-supplemented medium. The highest culturability was obtained using 300 mM glucose-supplemented medium. Based on observations of ultrastructural changes in relation to the culturability data, the coccoid forms could be categorized into three stages: dying, viable but non-culturable and proliferating organisms. The optimal glucose concentration for H. pylori culture in this liquid medium culture experiment was approximately 300 mM.

Expression profiling of responses of Helicobacter pylori to acidic media

metaplasia ([M) in patients from a high risk area of GC. Methods: We studied 101 patients who underwent endoscopy with (48 cases) or without (53 controls) GA and [M. All patients signed a valid consent, and blood samples were obtained prior endoscopy. Gastric biopsies were obtained from the antrum, body, and fundns. H. pylori culture was intended in all patients, from antrum and body biopsy samples. DNA was extracted and purified from one of the antrum biopsy for PCR analysis of several bacterial genes, including glmM, vacA and cagA as previously described (PNAS, 2002;99:15107-15111). Histology was performed for a single pathologist, who scored one biopsy for each of the three sites selected according to the Sidney system. Results: We found similar proportions of H. pylon positive individuals based on histology (81.1%) and serology (77.2%) in the whole group. Presence of GA and/ or IM was not associated with the presence of cagA+ strains (p=0.71), but was associated with infection by vacA sl strains (p = 0.03). H. pylon was more prevalent in patients without than in patients with GA or IM, when the status was defined by a serological criteria in combination with PCR amplification of glmM gene (p<0.01). No difference in age was observed between H. pylon positive and H. pylon negative patients; however, as expected, patients with GA or IM were older than patients without GA or IM (p<0.01), independently of H. pylori status. Conclusions: H. pylori prevalence was universally high in this community. Infection by vacA sl strains ks a risk factor for GA or IM, which are progression steps towards GC. Patients with intact gastric mucosa are more likely to be H. pylori positive, confirming that the progression in the gastric damage (GA and IM) modified the microenvironment for H. pylori.

Use of fluorescent in situ hybridization to evidence the presence of Helicobacter pylori in water

We have evaluated the use of a fluorescent in situ hybridization (FISH) technique for the detection of Helicobacter pylori in water (river and wastewater) samples. The assay was compared with PCR detection and isolation of cells on selective media. 16S rRNA and UreA+B sequence data were used as oligonucleotide probe and specific primers for FISH and PCR, respectively. Using FISH technique, H. pylori was detected in two river water and one wastewater samples, while PCR yielded only one positive result. H. pylori culture was not possible from any sample. According to these results, FISH technique has the potential to be used as a quick and sensitive method for detection of H. pylori in environmental samples.

Virulence of water-induced coccoidHelicobacter pyloriand its experimental infection in mice

To explore the virulence and the infectivity of coccoid Helicobacter pylori (H. pylori) transformed from spiral form by exposure to sterile tap water. Three strains of H. pylori, isolated from gastric biopsy specimens of confirmed peptic ulcer, were converted from spiral into coccoid form by exposure to sterile tap water. Both spiral and coccoid forms of H. pylori were tested for the urease activity, and the adherence to Hep-2 cells. The presence of flagella was examined under electron microscopy. In the experimental animal infection, the spiral and coccoid forms of H. pylori originated from the same strain F49 were inoculated intragastrically into BALB/c mice respectively four times at a 3-day interval. Half of the mice from each group were sacrificed at Day 21 and Day 28 after the last inoculation. Histology and H. pylori colonization were detected by urease test of gastric mucosa, cultures of H. pylori, and electron microscopy and so on. The urease activity and the ability of adherence to Hep-2 cells were found to be lower in coccoid H. pylori than that in its spiral form. For example, the transformation in strain F(44) led to a significant decrease of the adherence rate and adherence index from 70.0+/-5.3 % to 30.2+/-3.5 % (P<0.01), and from 2.6+/-0.4 to 0.86+/-0.3 (P<0.01), respectively. The flagella of coccoid H. pylori were observed under electron microscope. In the experimental infection in mice, the positive rate of gastric mucosa urease test was 93.8 % (15/16) in the group infected by spiral H. pylori and 50 % (8/16) in the group infected by coccoid H. pylori, and the estimated coccoid H. pylori colony number was 1.75 vs 0.56. The positive rates of H. pylori culture were 87.5 % (14/16) in spiral H. pylori group and 68.8 % (11/16) in coccoid H. pylori group. There was no significant difference in either urease test or bacterial culture rate between the groups examined at Day 21 and Day 28 after inoculation. Electron microscopic examination of the samples taken from both groups showed the adherence of H. pylori in spiral, bacillary and coccoid shapes to the epithelial cells of gastric wall. Histological examination showed the occurrence of gastric mucosal injury as indicated by various degrees of erosion, ulcer, and inflammatory cell infiltration. Mucosal injury was slighter in the mice infected by coccoid H. pylori. No positive result was obtained in the control group that received intragastrical administration of sterile tap water. Although the virulence of coccoid H. pylori induced by water decrease, coccoid H. pylori still remains a considerable urease activity and the adhering ability to epithelial cells. Furthermore, the flagella, an important component responsible for bacterial movement and infection, were still observed as a cellular structure of coccoid H. pylori under electron microscope. The coccoid H. pylori induced by water is capable of colonizing in gastric mucosa and causing gastrititis in mice.

Helicobacter pylori Genotypes in Israeli Children: The Significance of Geography

ABSTRACTBackgroundThere is substantial genetic variation among different isolates of Helicobacter pylori, which may affect the clinical outcome. The aims of this study were to find the common H. pylori genotypes in Israeli children and to look for a possible genotype–phenotype correlation.MethodsNinety‐eight H. pylori cultures were isolated from antral biopsy specimens of symptomatic Israeli children and were analyzed for vacA and iceA genotype and cagA and cagE status by polymerase chain reaction.ResultscagA and cagE genes were present in only 25.5% and 24.5%, respectively. The common vacA genotype was s2m2, which was found in 65%. Eleven specimens (11%) contained multiple vacA genotypes. iceA1 was found in 37% and iceA2 in 52% of cases. Both iceA alleles were found in 11%. Increased prevalence of iceA1 and cagE were observed in children with duodenal disease, although it did not reach significance.ConclusionsThe low prevalence of cagA and the high prevalence of vacA genotype s2m2 in Israeli pediatric patients are different from the genotype prevalence reported globally. However, similar findings have been reported in Egypt, indicating a possible geographic influence. There is a possible correlation between duodenal ulcer and cag E and ice A1 genotype, but the power of the study was too low to prove it.

Helicobacter pylori genotypes in Israeli children: the significance of geography.

There is substantial genetic variation among different isolates of Helicobacter pylori, which may affect the clinical outcome. The aims of this study were to find the common H. pylori genotypes in Israeli children and to look for a possible genotype-phenotype correlation. Ninety-eight H. pylori cultures were isolated from antral biopsy specimens of symptomatic Israeli children and were analyzed for vacA and iceA genotype and cagA and cagE status by polymerase chain reaction. cagA and cagE genes were present in only 25.5% and 24.5%, respectively. The common vacA genotype was s2m2, which was found in 65%. Eleven specimens (11%) contained multiple vacA genotypes. iceA1 was found in 37% and iceA2 in 52% of cases. Both iceA alleles were found in 11%. Increased prevalence of iceA1 and cagE were observed in children with duodenal disease, although it did not reach significance. The low prevalence of cagA and the high prevalence of vacA genotype s2m2 in Israeli pediatric patients are different from the genotype prevalence reported globally. However, similar findings have been reported in Egypt, indicating a possible geographic influence. There is a possible correlation between duodenal ulcer and cag E and ice A1 genotype, but the power of the study was too low to prove it.

Effect of Helicobacter pylori on delay in ulcer healing induced by aspirin in rats

Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) are major pathogenic factors in peptic ulcer disease but whether these two factors exert synergistic or antagonistic effects on ulcer healing has been a subject of controversy. We compared the effect of aspirin alone with that of aspirin combined with H. pylori on gastric acid secretion and healing of acetic acid gastric ulcers in rats. The H. pylori colonization of gastric mucosa was determined by viable H. pylori culture, histology and assessment of bacterial DNA using polymerase chain reaction (PCR). The area of ulcers, gastric blood flow, mucosal generation of prostaglandin E 2 and plasma gastrin levels and expression of cyclooxygenase-1, cyclooxygenase-2 and growth factors was determined. Aspirin delayed significantly the healing of chronic gastric ulcers, decreased the gastric blood flow at the ulcer margin and gastric mucosal prostaglandin E 2 generation being without significant influence on gastric acid output. H. pylori acquisition that produced moderate gastric inflammation at the ulcer margin delayed significantly the healing of gastric ulcers, decreased significantly both the gastric blood flow at the ulcer margin and the gastric secretion while raising significantly the gastric mucosal prostaglandin E 2 generation and plasma gastrin levels. H. pylori infection attenuated the aspirin-induced inhibition of ulcer healing and accompanying fall in the gastric blood flow. Both aspirin and H. pylori up-regulated significantly cyclooxygenase-2 messenger RNA (mRNA) and protein but not that of cyclooxygenase-1 at the ulcer margin. Aspirin reduced significantly the transforming growth factor alpha- and vascular endothelial growth factor mRNAs, but these effects were significantly attenuated by H. pylori. We conclude that H. pylori antagonizes, in part, aspirin-induced delay of ulcer healing due to suppression of acid secretion, the enhancement in prostaglandin E 2 possibly derived from cyclooxygenase-2 and the overexpression of transforming growth factor alpha and vascular endothelial growth factor in the ulcer area.

Floating-Bioadhesive Microspheres Containing Acetohydroxamic Acid for Clearance of Helicobacter Pylori

A new strategy based on gastric retention is proposed for the treatment of Helicobacter pylori. (H. pylori) . A synergism between a floating and a bioadhesive system has been explored. Floating microspheres containing the antiurease drug acetohydroxamic acid (AHA) were prepared by a novel quasi-emulsion solvent diffusion method. The microballons were characterized for size distribution, morphology, drug content, drug release, and in vitro floating property. The microballons were coated with 2% w/v solution of polycarbophil by the air suspension coating method. The bioadhesive property of the microspheres was investigated by the detachment force measurement method. In vitro growth inhibition studies were performed in isolated H. pylori culture. The results suggest that AHA-loaded floating microspheres are superior as potent urease inhibitors whereas urease plays an important role in the colonization of H. pylori. We suggest that an oral dosage containing floating-bioadhesive microspheres may form a useful drug delivery system for the treatment of H. pylori.

Comparison of Three 7-Day Pantoprazole-Based Helicobacter pylori Eradication Regimens in a Mexican Population with High Metronidazole Resistance

To compare the efficacy and tolerability of three 7-day pantoprazole-based regimens to eradicate Helicobacter pylori in Mexican patients with peptic ulcer (PU) or non-ulcer dyspepsia (NUD). Short-term therapeutic regimens based on a proton pump inhibitor (PPI) and two antibiotics have been recommended for the eradication of H. pylori. Resistance of H. pylori to metronidazole may adversely affect the efficacy of such regimens. This was a single-centre, randomised, open-label, parallel-group study in which three groups of H. pylori-positive patients with PU or NUD were compared (n = 159; intention-to-treat population). Patients were randomised to receive a 7-day pantoprazole-based triple therapy for eradication of H. pylori. Patients received pantoprazole (P) 40mg twice daily in combination with either i) amoxicillin (A) 1000mg twice daily and clarithromycin (C) 500mg three times daily (PAC regimen, n = 51 patients), or ii) clarithromycin 500mg three times daily and metronidazole (M) 500mg three times daily (PCM regimen, n = 55 patients), or iii) amoxicillin 1000mg twice daily and metronidazole 500mg three times daily (PAM regimen, n = 53 patients). After completing eradication therapy, all PU patients were further treated with once-daily pantoprazole 40mg, either for another 3 weeks (patients with duodenal ulcer) or for another 7 weeks (patients with gastric ulcer), to ensure complete ulcer healing. At baseline examination, all patients underwent the (14)C-urea breath test and endoscopy; biopsy specimens were taken for histology, CLO-test, H. pylori culture and antibiotic susceptibility testing (agar dilution E-test). Eradication of H. pylori was assessed after all treatment with pantoprazole had been discontinued for at least 4 weeks, using the (14)C-urea breath test. In the per-protocol population (n = 153), eradication was achieved in 81.3% (39/48) of patients receiving PAC, 66.0% (35/53) of PCM recipients, and 48.1 % (25/52) of those receiving PAM (p = 0.13 for PAC vs PCM and 0.001 for PAC vs PAM). In the intention-to-treat population, respective eradication rates were 76.5 (39/51), 63.6 (35/55) and 47.2% (25/53) [p = 0.22 for PAC vs PCM and 0.004 for PAC vs PAM]. Patient compliance was very good in all treatment groups. The main adverse event affecting 40% of all patients was a metallic taste, assessed as likely related to the antibiotics. Susceptibility to the three study antibiotics was determined for H. pylori isolates using the pretreatment biopsies from 103 patients. Resistance to metronidazole was present in 68.2% of patients and to clarithromycin in 24.3%. In 16.8% of patients, H. pylori isolates were resistant to both metronidazole and clarithromycin. In patient populations with H. pylori strains resistant to one or both of the antibiotics used in the respective treatment regimen, eradication rates were consistently lower than in those with susceptible H. pylori strains. However, these differences were not statistically significant, probably due to the small sample size. The 7-day H. pylori eradication regimen with PAC was superior to PCM and PAM. This is probably due to the high resistance rate to metronidazole in the Mexican population. Thus, H. pylori eradication regimens that involve metronidazole cannot be recommended for Mexican patients. RESULTS from this study highlight the regional differences in efficacy of some well established H. pylori eradication regimens, and suggest that culture and susceptibility testing to define H. pylori resistance patterns in specific geographical areas may be indicated before recommending any particular eradication schedule.

Noninvasive stool antigen assay can effectively screen Helicobacter pylori infection and assess success of eradication therapy in hemodialysis patients

Helicobacter pylori (H pylori) stool antigen (HpSA), serological antibody against H pylori (immunoglobulin G [IgG]), and urea breath test (UBT) are noninvasive methods used to detect H pylori infection that can allow a patient to avoid the discomfort and risk of invasive endoscopy. However, because the UBT has proven not highly reliable in patients with end-stage renal disease (ESRD), this study attempts to investigate the diagnostic efficacy of HpSA and IgG for H pylori detection in 80 patients with ESRD and 80 dyspeptic patients without renal function impairment as a control group. All patients in both study groups underwent panendoscopy to obtain gastric biopsy specimens for histological examination and H pylori culture. With H pylori infection defined as a positive result on either histological examination or culture, we evaluated the reliability of HpSA and serum IgG in detecting H pylori infection. Forty of the patients with ESRD (50%) and 48 patients in the control group (60%) were proven to be infected with H pylori. To eradicate H pylori infection, these patients were administered a 1-week course of triple therapy. To evaluate the success of H pylori eradication, 38 patients in the ESRD group and 44 patients in the control group underwent a follow-up endoscopy and provided stool samples for HpSA 6 to 8 weeks later. Success of H pylori eradication was found in 86.8% of the patients with ESRD (33 of 38 patents) and 84.1% of the control patients (37 of 44 patients). Before therapy, HpSA for H pylori detection was 97.5% sensitive and 97.5% specific in patients with ESRD, as effective as that in the control group. After therapy, HpSA was 100% sensitive and more than 96% specific to detect the failure of H pylori eradication therapy in both the ESRD and control groups. Conversely, the use of IgG as a screening method for H pylori infection proved to be less effective because it showed a sensitivity of 87.5% and specificity of 80% in this study. Monitoring the success of triple therapy, IgG had a specificity of only 21.9% in the ESRD group and 24.3% in the control group. In summary, HpSA is a noninvasive and reliable tool to screen H pylori infection before therapy and assess the success of eradication therapy in patients with ESRD. © 2001 by the National Kidney Foundation, Inc.

Inhibitory actions of luteolin on the growth and arylamine N-acetyltransferase activity in strains of Helicobacter pylori from ulcer patients

Helicobacter pylori is now recognized as an important cause of type B gastritis, which is strongly associated with gastric and duodenal ulcer disease. H. pylori may be a causative factor in patients with gastric cancer. The growth inhibition and N-acetylation of 2-Aminofluorene (AF) or P-aminobenzoic acid (PABA) by arylamine N-acetyltransferase (NAT) in H. pylori were inhibited by luteolin, a component in herbal medicine. The growth inhibition was based on the changes of optical density (OD) by using a spectrophotometer. The N-acetylation of AF or PABA by NAT from H. pylori were assayed by the amounts of acetylated and non-acetylated AF or PABA in cytsols and intact bacteria of H. pylori by using HPLC. An inhibition of growth on H. pylori demonstrated that luteolin elicited a dose-dependent growth inhibition in the H. pylori cultures. Cytosols and suspensions of H. pylori with or without specific concentrations of luteolin co-treatment showed different percentages of AF or PABA acetylation. The data indicated that there was decreased NAT activity associated with increased levels of luteolin in H. pylori cytosols and suspensions. Using standard steady-state kinetic analysis, it was demonstrated that luteolin was a possible uncompetitive inhibitor to NAT enzyme in H. pylori. This report is the first demonstration to show that luteolin can inhibit H. pylori growth and NAT activity.