Endoscopy Is Cost-Effective for Gastric Cancer Screening After Successful Helicobacter pylori Eradication.

BACKGROUND: After successful Helicobacter pylori eradication, patients with gastric mucosal atrophy are at high risk of gastric cancer. Endoscopy can detect early gastric cancer with high sensitivity. AIMS: This study aimed to assess the cost-effectiveness of annual endoscopy versus biennial endoscopy versus no screening for gastric cancer screening in patients after successful Helicobacter pylori eradication. METHODS: We developed decision trees with Markov models for a hypothetical cohort of patients aged 50 years after successful Helicobacter pylori eradication over a lifetime horizon from a healthcare payer perspective. Main outcomes were costs, quality-adjusted life-years (QALYs), life expectancy life-years (LYs) with discounting at a fixed annual rate of 3%, and incremental cost-effectiveness ratios (ICERs). RESULTS: In a base-case analysis, biennial endoscopy (US$4305, 19.785QALYs, 19.938LYs) was more cost-effective than annual endoscopy (US$7516, 19.808QALYs, 19.958LYs, ICER; US$135,566/QALY gained) and no screening (US$14,326, 19.704QALYs, 19.873LYs). In scenario analyses, biennial endoscopy for patients with mild-to-moderate gastric mucosal atrophy and annual endoscopy for patients with severe gastric mucosal atrophy were the most cost-effective. Cost-effectiveness was sensitive to incidence of gastric cancer and the proportion of stage I. Probabilistic sensitivity analyses using Monte Carlo simulation demonstrated that at a willingness-to-pay level of US$100,000/QALY gained, biennial endoscopy was optimal 99.9% for patients with mild-to-moderate gastric mucosal atrophy, and that annual endoscopy was optimal 98.4% for patients with severe gastric mucosal atrophy. CONCLUSIONS: Based on cancer risk assessment of gastric mucosal atrophy and cost-effectiveness results, annual or biennial endoscopic surveillance could be established for patients after successful Helicobacter pylori eradication.

Education and gastric cancer risk-An individual participant data meta-analysis in the StoP project consortium.

Low socioeconomic position (SEP) is a strong risk factor for incidence and premature mortality from several cancers. Our study aimed at quantifying the association between SEP and gastric cancer (GC) risk through an individual participant data meta-analysis within the "Stomach cancer Pooling (StoP) Project". Educational level and household income were used as proxies for the SEP. We estimated pooled odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) across levels of education and household income by pooling study-specific ORs through random-effects meta-analytic models. The relative index of inequality (RII) was also computed. A total of 9,773 GC cases and 24,373 controls from 25 studies from Europe, Asia and America were included. The pooled OR for the highest compared to the lowest level of education was 0.60 (95% CI, 0.44-0.84), while the pooled RII was 0.45 (95% CI, 0.29-0.69). A strong inverse association was observed both for noncardia (OR 0.39, 95% CI, 0.22-0.70) and cardia GC (OR 0.47, 95% CI, 0.22-0.99). The relation was stronger among H. pylori negative subjects (RII 0.14, 95% CI, 0.04-0.48) as compared to H. pylori positive ones (RII 0.29, 95% CI, 0.10-0.84), in the absence of a significant interaction (p = 0.28). The highest household income category showed a pooled OR of 0.65 (95% CI, 0.48-0.89), while the corresponding RII was 0.40 (95% CI, 0.22-0.72). Our collaborative pooled-analysis showed a strong inverse relationship between SEP indicators and GC risk. Our data call for public health interventions to reduce GC risk among the more vulnerable groups of the population.

Burden of disease from Helicobacter pylori infection in western Canadian Arctic communities.

BACKGROUND: Indigenous communities across the circumpolar north have elevated H. pylori (Hp) prevalence and stomach cancer incidence. We aimed to describe the Hp-associated disease burden among western Canadian Arctic participants in community-driven projects that address concerns about health risks from Hp infection. METHODS: During 2008-2013, participants underwent Hp screening by urea breath test and gastroscopy with gastric biopsies. We estimated Hp prevalence and prevalence by Hp status of endoscopic and histopathologic diagnoses. RESULTS: Among 878 participants with Hp status data, Hp prevalence was: 62% overall; 66% in 740 Indigenous participants; 22% in 77 non-Indigenous participants (61 participants did not disclose ethnicity); 45% at 0-14 years old, 69% at 15-34 years old, and 61% at 35-96 years old. Among 309 participants examined endoscopically, visible mucosal lesions were more frequent in the stomach than the duodenum: the gastric to duodenal ratio was 2 for inflammation, 8 for erosions, and 3 for ulcers. Pathological examination in 308 participants with gastric biopsies revealed normal gastric mucosa in 1 of 224 Hp-positive participants and 77% (65/84) of Hp-negative participants with sharp contrasts in the prevalence of abnormalities between Hp-positive and Hp-negative participants, respectively: moderate-severe active gastritis in 50 and 0%; moderate-severe chronic gastritis in 91 and 1%; atrophic gastritis in 43 and 0%; intestinal metaplasia in 17 and 5%. CONCLUSIONS: The observed pattern of disease is consistent with increased risk of stomach cancer and reflects substantial inequity in the Hp-associated disease burden in western Arctic Canadian hamlets relative to most North American settings. This research adds to evidence that demonstrates the need for interventions aimed at reducing health risks from Hp infection in Indigenous Arctic communities.

Upfront special staining for Helicobacter pylori in gastric biopsy specimens is not indicated.

OBJECTIVES: The practice of routine upfront use of special stains in biopsy specimens with minimal or no inflammation has not been evaluated. This study was conducted to determine the value of special stains for Helicobacter pylori in gastric biopsy specimens showing variable degrees of inflammation and to evaluate the practice of upfront ancillary staining of all mucosal biopsy specimens. METHODS: Immunohistochemical or Diff-Quik stains were done on sections of 570 gastric biopsy specimens. The rates of positivity for H pylori were calculated in each category based on the degree of inflammation and classified as normal, minimal, mild, moderate, or severe. RESULTS: H pylori was not detected in 386 (67.7%) biopsy specimens that were classified as normal (6.0%) or with minimal inflammation (28.2%) or mild inactive gastritis (33.5%). The organism was identified by Diff-Quik or immunohistochemical stain in 76 (89.4%) of 85 with moderate active gastritis and 30 (93.8%) of 32 biopsy specimens showing severe active gastritis. CONCLUSIONS: Upfront staining of gastric biopsy specimens is not cost-effective since a significant proportion of the gastric biopsy specimens were normal or showed minimal inflammation; in none of these biopsy specimens was the organism found. Special stains should be performed only in selected biopsy specimens that reveal any degree of chronic active gastritis or moderate inactive gastritis.

Helicobacter pylori eradication for preventing gastric cancer.

Helicobacter pylori (H. pylori) infection is a major risk factor for gastric cancer (GC) development, which is one of the most challenging malignant diseases worldwide with limited treatments. In the multistep pathogenesis of GC, H. pylori infection slowly induces chronic active gastritis, which progresses through the premalignant stages of atrophic gastritis, intestinal metaplasia, and dysplasia, and then finally to GC. Although eradication of H. pylori is a reasonable approach for the prevention of GC, there have been some contradictory reports, with only some long-term follow-up data showing efficacy of this approach. The inconsistencies are likely due to the insufficient number of participants, relatively short follow-up periods, poor quality of study designs, and the degree and extent of preneoplastic changes at the time of H. pylori eradication. This review analyzes recent high-quality studies to resolve the discrepancies regarding the eradication of H. pylori for GC prevention. The relationship between H. pylori eradication and GC/precancerous lesions/metachronous GC is examined, and the cost-effectiveness of this strategy in the prevention of GC is assessed. Although it is assumed that eradication of H. pylori has the potential to prevent GC, the feasibility and appropriate timing of this strategy for cancer prevention remain to be determined. As a result, additional well-designed trials with longer follow-up periods are needed to clarify this issue.

Assessment of the relationship between Helicobacter pylori infection, endoscopic appearance and histological changes of the gastric mucosa in children with gastritis (a single center experience).

BACKGROUND: Helicobacter pylori infection is an important cause of gastritis in childhood, its role in the pathogenesis of peptic ulcer disease in adults and children being generally known. In some cases, there are therapeutic management issues, because they do not heal or they often relapse, although treatment regimens are applied as recommended. Our aim was to analyze the relationship between endoscopic appearance and histological changes of the gastric mucosa in children with gastritis associated with H. pylori infection, in which persistent infection after treatment was found. MATERIALS AND METHODS: It was a prospective study on 1332 children assessed in our Service (Ist Pediatric Clinic, Tirgu Mures, Romania), between January 2008 and January 2013, for gastritis with various etiologies. There were 609 cases of gastritis-associated with H. pylori infection. RESULTS: The average age of patients was 13.21 years; the higher incidence was noted in 13-18-year-old group, female gender and rural areas provenience; a number of 544 patients diagnosed with gastritis with H. pylori were reassessed subsequently; after treatment, gastritis has healed and the infection was eradicated in 88.23% cases after a month, while in 64 patients infection persisted. After a second regimen, endoscopic-histological modifications persisted in 31 (5.69%) cases; 1.28% cases remained positive for longer. CONCLUSIONS: H. pylori infection was associated with high age group, as well as with endoscopic modifications; also, the presence of H. pylori was correlated with histopathologic diagnostic. We try to emphasize the importance of assessing bacterial resistance to antibiotics, studying of bacterial genome and genetic susceptibility of human subjects.

Assessment of Helicobacter pylori eradication in patients on NSAID treatment.

BACKGROUND: In this post-hoc analysis of a randomized, double blind, placebo controlled trial, we measured the sensitivity and specificity of Helicobacter pylori IgG-antibody titer changes, hematoxylin and eosin (H&E) stains, immunohistochemical (IHC) stains and culture results in NSAID using patients, following H. pylori eradication therapy or placebo. METHODS: 347 NSAID using patients who were H. pylori positive on serological testing for H. pylori IgG-antibodies were randomized for H. pylori eradication therapy or placebo. Three months after randomization, gastric mucosal biopsies were taken for H. pylori culture and histological examination. At 3 and 12 months, blood samples were taken for repeated serological testing. The gold standard for H. pylori infection was based on a positive culture or both a positive histological examination and a positive serological test. Sensitivity, specificity and receiver operating curves (ROC) were calculated. RESULTS: H. pylori eradication therapy was successful in 91% of patients. Culture provided an overall sensitivity of 82%, and 73% after eradication, with a specificity of 100%. Histological examination with either H&E or IHC stains provided sensitivities and specificities between 93% and 100%. Adding IHC to H&E stains did not improve these results. The ROC curve for percent change in H. pylori IgG-antibody titers had good diagnostic power in identifying H. pylori negative patients, with an area under the ROC curve of 0.70 (95 % CI 0.59 to 0.79, P = 0.085) at 3 months and 0.83 (95% CI 0.76 to 0.89, P < 0.0001) at 12 months. A cut-off point of at least 21% decrease in H. pylori IgG-antibody titers at 3 months and 58% at 12 months provided a sensitivity of 64% and 87% and a specificity of 81% and 74% respectively, for successful eradication of H. pylori. CONCLUSIONS: In NSAID using patients, following H. pylori eradication therapy or placebo, histological examination of gastric mucosal tissue biopsies provided good sensitivity and specificity ratios for evaluating success of H. pylori eradication therapy. A percentual H. pylori IgG-antibody titer change has better sensitivity and specificity than an absolute titer change or a predefined H. pylori IgG-antibody titer cut-off point for evaluating success of H. pylori eradication therapy.

Assessment of desmosomal components (desmoglein 1-3, plakoglobin) in cardia mucosa in relation to gastroesophageal reflux disease and Helicobacter pylori infection.

Gastroesophageal reflux disease is associated with impaired epithelial barrier function and abnormal expression of proteins forming cell-cell contacts by tight junctions and desmosomes in distal esophageal squamous mucosa. Although gastroesophageal reflux disease and Helicobacter pylori are both associated with chronic inflammation of the adjacent cardia mucosa, it is not known whether these lead to derangements of the desmosomal complexes. Here, we assessed the expression of 4 proteins (plakoglobin and desmoglein 1, 2, and 3) forming epithelial desmosomal complexes by quantitative reverse transcription polymerase chain reaction and immunohistochemistry in biopsies from 67 patients with gastroesophageal reflux disease and 23 gastroesophageal reflux disease-negative controls. Plakoglobin and desmoglein 2 were ubiquitously expressed in all samples, whereas desmoglein 1 and 3 were not expressed in cardia mucosa. Gastroesophageal reflux disease was specifically associated with elevated transcript levels of desmoglein 2 and plakoglobin. These were significantly increased from 2.0- to 2.7-fold in patients with gastroesophageal reflux disease compared with controls (P < .01), and significantly increased immunohistochemical scores for both proteins were observed (P < .05) as well. The combined presence of gastroesophageal reflux disease and Helicobacter pylori infection had no additional effect on desmosomal gene expression. Taken together, the up-regulation of plakoglobin and desmoglein 2 in cardia mucosa of patients with gastroesophageal reflux disease supports the concept that the "transition zone" between distal esophagus and proximal stomach is affected by gastroesophageal reflux disease as well, and architectural and molecular changes in the desmosomal compartment contribute to the pathogenesis of gastroesophageal reflux disease in the cardia mucosa.

[Time course of gastric mucosal changes in the assessment of long-term results of Helicobacter pylori eradication].

The impact of Helicobacter pylori (H. pylori) eradication on the gastric mucosa (GM) was studied in patients with gastroduodenal ulcers. Clinical and morphological changes in the GM were assessed in 122 patients 3-7 years (mean 4.4 +/- 1.3 years) after eradication therapy and in 12 patients who had undergone H. pylori eradication. Successful H. pylori eradication in the gastric antral and body mucosa reduced inflammation, the degree of chronic inflammation, the number of lymphoid follicles, and the magnitude of gland atrophy. There were no statistically significant changes in intestinal metaplasia. The patients who had not received eradication therapy showed no significant GM changes as compared to the baseline values. In the unsuccessful eradication group, inflammation statistically significantly diminished in the gastric antrum and body with a reduction in the density of H. pylori contamination.

Vaccinating against Helicobacter pylori infection.

Helicobacter pylori infection of the gastric mucosa remains a cause of significant morbidity and mortality almost 30 years after its discovery. H. pylori infection can lead to several gastric maladies, including gastric cancer, and although antimicrobial therapies for the infection exist, the cost of treatment for gastric cancer and the prognosis of individuals who present with this disease make vaccine development a cost effective alternative to bacterial eradication. Experimental mucosal and systemic H. pylori vaccines in mice significantly reduce bacterial load and sometimes provide sterilizing immunity. Clinical trials of oral vaccines consisting of H. pylori proteins with bacterial exotoxin adjuvants or live attenuated bacterial vectors expressing H. pylori proteins induce adaptive immune mechanisms but fail to consistently reduce bacterial load. Clinical trials and murine studies demonstrate that where H. pylori is killed, either spontaneously or following vaccination, the host demonstrated cellular immunity. Improved efficacy of vaccines may be achieved in new trials of vaccine formulations that include multiple antigens and use methods to optimize cellular immunity. Unfortunately, the industrial sponsors that served as the primary engine for much of the previous animal and human research have withdrawn their support. A renewed or expanded commitment from the biotechnology or pharmaceutical industry that could exploit recent advances in our understanding of the host immune response to H. pylori is necessary for the advancement of an H. pylori vaccine.

Detection of Helicobacter pylori: A faster urease test can save resources.

AIM: To investigate whether differences in the rapidity of a positive result for Helicobacter pylori can save resources, by comparing two commercially available urease kits. METHODS: One hundred and eighty-five adults (130 outpatients, 55 inpatients) undergoing gastroscopy were entered prospectively. Patients were divided into two groups: Group 1 (if they were not on PPIs, antibiotics, H2A, bismuth or sucralfate for up to 14 d prior to the endoscopy) and Group 2 (if they were on, or had been on, any of the above medication in the previous 14 d). At endoscopy two sets of biopsies, taken in random order, were placed in the wells of the Campylobacter-like organism (CLO) test (Kimberly-Clark, Utah, USA) and the Quick test (Biohit Plc, Helsinki, Finland). Five additional gastric biopsies were taken for histology/Giemsa and immunohistochemical study. The two urease test slides were read at 2 min, 30 min, 2 h and 24 h. Sensitivity and specificity at 24 h were determined. RESULTS: At 24 h, for all patients, there was no difference in sensitivity (100% vs 97.5%), specificity (99.3%), positive (97.5%) and negative predictive values (100% vs 99.3%) between the CLO and Quick tests, respectively. There was a positive result at 30 min in 17/41 (41.5%) CLO tests, and in 28/40 (70%) Quick tests, P = 0.05. Quick test enabled the prescription of eradication therapy before discharge in all 28/40 patients. Only 12 (30%) follow-up appointments were needed. If the CLO test had been used alone, only 17 (41.5%) prescriptions would have been possible prior to discharge and 24 (58%) follow-up appointments would be needed (P = 0.001). Of 2000 gastroscopies performed annually at our unit, a saving of 123 follow-up appointments (total: 8856 Euros or 11 808 USD) would be achieved if we switched to the Quick test. CONCLUSION: Direct comparison of locally available urease test kits is worthwhile, since the appropriate choice results in a significant saving of resources. Local costs and follow-up protocols will determine the magnitude of these savings.

Assessment of co-existence of Helicobacter pylori and Candida fungi in diseases of the upper gastrointestinal tract.

Candida spp. were found in the gastric mucosa of 27 (17%) patients, out of whom 18 (11%) showed co-existence of the fungi with H. pylori. Analysis of relationship between selected disorders of the upper gastrointestinal tract (non ulcer dyspepsia NUD, gastric ulcer, duodenal ulcer) and infection with H. pylori and/or Candida revealed a link between co-existence of H. pylori with Candida and gastric ulcers suggesting synergism of those microorganism in pathogenesis of the disease. On the contrary, according to quantitative studies performed, the fungi alone do not play a significant role in pathogenesis of the above mentioned disorders as they colonize only epithelium to the extent that is not pathologically significant (<10(3) CFU/ml). Genetical study was carried out on 57 Helicobacter pylori strains isolated from bioptates of the gastric mucosa. The genotypes of the strains (gene cagA and alleles of gene vacA - m1, m2, s1, s2) were determined using the PCR technique. As it was shown, the patients infected with H. pylori strains of genotype cagA+, vacA s1 are exposed to higher risk of peptic ulcer disease (PUD) as compared to the patients infected with cagA-, vacA s2 strains. In the case of the NUD patients a correlation with allele m2 was found only (p<0.001). This may suggest that in future some of the NUD patients infected with cagA+, vacA s1 strains will fall into the group at higher risk for PUD.

[Assessment of rate of hydroxyl anions production by Helicobacter pylori in stomach].

Production of hydroxyl anions by tissue samples of pylorus mucous membrane obtained from 45 patients with gastric or duodenal ulcers was investigated. The production was estimated using the recently developed method based on measurement of rate of pH change in urea-containing reaction mixture. The rate of [OH-] generation as a result of H. pylori metabolism accounted on pylorus square varied from 0.4 to 1318.9 mcmol [OH-]/min, and in 90.2% of cases it did not exceed 128.1 mcmol [OH-]/min. This rate is comparable to mean rate of [H+] generation in stomach of healthy man--114.2-238.4 mcmol [H+]/min. Obtained results allow to conclude that this bacterium may participate in regulation of stomach acid-base balance.

[The assessment of nitric oxide metabolites in gastric juice in Helicobacter pylori infected subjects in compliance with grade of inflammatory lesions in gastric mucosa]. / Ocena stezenia metabolitów tlenku azotu w soku zoladkowym u zakazonych Helicobacter pylori z uwzglednieniem stopnia zmian zapalnych w blonie sluzowej zoladka.

UNLABELLED: The infection of H. pylori causes inflammatory lesions in gastric mucosa--until atrophic gastritis, intestinal metaplasia, dysplasia (precancerous states) and finally to gastric cancer or lymphoma. The mechanism of mentioned disturbances is complicated, no doubt that nitric oxide plays here very important role. It is proved, that H. pylori causes essential oxygen metabolism disturbances by activation of inflammatory infiltration's cells to oxide reactive forms as nitric oxide formation. Nitric oxide as oxide radical could react with other free radicals and contribute to oxidative lesions of gastric mucosa and alterations of its structure. The aim of the study was try to answer the question: 1. Is this the relationship between NO metabolites concentrations in gastric juice and morphological state of gastric mucosa? 2. Does H. pylori eradication influence on NO metabolites concentrations in gastric juice? 3. Does H. pylori eradication influence on grade of inflammatory lesions in gastric mucosa? MATERIAL AND METHODS: The study included 75 subjects between of 21 to 60 years, infected with H. pylori with diagnosed (according to the Sydney system) different stages of chronic gastritis progression. The type of inflammation, activity, the presence of atrophy, intestinal metaplasia and H. pylori infection were assessed. The study group was divided into 3 subgroups: group I--25 subjects with chronic active gastritis, group II--25 subjects with chronic atrophic gastritis without intestinal metaplasia, group III--25 subjects with chronic atrophic gastritis with intestinal metaplasia. Control group comprised 20 healthy subjects, without H. pylori infection. In each patient during gastroscopy 5 biopsy specimens for histopathologic examination and for urea test and 3 ml gastric juice were collected. The concentration of nitric oxide metabolites in gastric juice was determined with spectrophotometric method, based on Griess reaction. H. pylori infection was detected using fast urea test (CLO--test), confirmed by histopathological examination (stained Giemsa method) and non-invasive urea breath test (UBT-13C). In H. pylori--infected patients the above mentioned investigations were performed three times -before, in 8 weeks and in 12 months after antibacterial treatment's finish. In antibacterial therapy we use 7-days three-drugs therapy (omeprasole, amoksycillin and clarythromycin). RESULTS: The concentration of nitric oxide metabolites in gastric juice in healthy subjects was 6.81 +/- 2.23 micromol. In patients with chronic gastritis, H. pylori infected was significantly higher--in patients with chronic active gastritis was 9.29 +/- 2.19 micromol/l, in patients with chronic atrophic gastritis--10.25 +/- 2.31 micromol/l (p < 0.01), in patients with intestinal metaplasia--11.89 +/- 2.46 micromol/l (p < 0.01). 8 weeks after antibacterial treatment's finish the concentration of nitric oxide metabolites in gastric juice in each group decreased and were: in patients with chronic active gastritis was 8.18 +/- 1.63 micromol/l, in patients with chronic atrophic gastritis--10.02 +/- 2.28 micromol/l, in patients with intestinal metaplasia--10.83 +/- 2.32 micromol/l. The differences were not statistically significant. 12 months after antibacterial treatment's finish the concentration of nitric oxide metabolites in gastric juice in each group decreased and were: in patients with chronic active gastritis was 6.90 +/- 1.43 micromol/l, in patients with chronic atrophic gastritis--7.22 +/- 2.01 micromol/l, in patients with intestinal metaplasia--7.56 +/- 1.98 micromol/l. The differences were statistically significant--p < 0.05, p < 0.01. 8 weeks after antibacterial treatment's finish in each patient also the gastroscopy was performed and another biopsy specimen for histopathologic examination were collected. Only in group I in microscopic image the decreased of inflammation intensity was find (both in antrum and in corpus)--however the differences were not statistically significant. In the other groups the alterations in gastric mucosa do not improve significantly. The gastroscopy was performed again in 12 months after antibacterial treatment's finish. In group I the significant decrease or regression of inflammatory infiltration (in corpus and in antrum) was found. Also in group II the significant decrease of the grade of atrophy and similarly in III group the improvement of histopathological state were observed. CONCLUSIONS: 1. The increase of NO metabolites concentration demonstrates positive correlation with grade of inflammatory lesions in gastric mucosa. 2. The effective antibacterial therapy causes the decrease of NO metabolites concentration in gastric juice, especially in patients with chronic active gastritis. 3. Eradication influence on decrease of grade of lesions' progression in gastric mucosa just in 12 months after effective antibacterial therapy.

Experimental model in the qualitative and quantitative assessment of non-Helicobacter gastric microflora under proton pump inhibitors action / Modelo experimental na avaliação qualitativa e quantitativa da microflora gástrica não-Helicobacter sob ação de inibidores de bomba de próton

PURPOSE: To evaluate models of gastric material collection from Wistar rats with and without using proton pump inhibitors(PPIs). METHODS: Twenty-four rats underwent intraperitoneal omeprazol treatment, and other 12 received similar treatment with 0.9 percent saline. All animals underwent collection of gastric material samples, after stomach removal, by either biopsies, or aspirates, or swabs. Samples were bacteriologically processed in order to identify species and strains. Values are described as natural logarithm of colony former units per mL [Ln(CFU/mL)]. Kruskal-Wallis and Mann-Whitney non-parametric tests were used, and p<0.05 was set as statistically significant. RESULTS: Significant difference was not seen for Ln (UFC/mL) values among the three methods of collection irrespective of using or not omeprazol. Also, significant difference was not seen in Ln (UFC/mL) values when comparing a method with each others, either using omeprazol or placebo. A significant increase of bacteria strains occurred when PPI was used, and this was seen on the three ways of collection, mainly in biopsy and swab. CONCLUSION: No difference occurred among the three methods of collecting bacteria samples from stomachs of rats, either when using placebo or omeprazol. A remarkable change is seen on animals bacterial microflora when PPIs are used, and bacteria are better identified when swab and biopsy are used.

OBJETIVO: Avaliar modelos de coleta de material gástrico de ratos da linhagem Wistar, com e sem o uso de inibidores de bomba de próton (IBPs). MÉTODOS: 24 ratos foram submetidos a tratamento com omeprazol intraperitoneal e 12 outros ratos receberam tratamento semelhante com solução salina a 0,9 por cento. Os animais foram submetidos a coleta de amostras de material gástrico, após retirada do estômago, utilizando-se de biópsias, aspirados ou swabs. Os materiais obtidos foram processados bacteriologicamente para identificação de espécimes quanto ao gênero. Os valores são descritos em logaritmo natural das unidades formadoras de colônias por mL [Ln(UFC/mL)]. Utilizou-se os testes não-paramétricos de Kruskal-Wallis e Mann-Whitney, considerando-se p<0,05 como estatisticamente significativo. RESULTADOS: Não se observou diferença significativa da quantidade de Ln(UFC/mL) entre os três métodos de coleta, independente do uso de omeprazol. Também não se observou diferença significativa de Ln(UFC/mL) ao comparar-se os métodos individualmente entre si nas condições de uso de omeprazol ou placebo. Houve aumento significativo da variedade de gêneros de bactérias com o uso de IBP, nos 3 métodos de coleta, sendo isto mais perceptível na biópsia e swab. CONCLUSÃO: Não houve diferença entre os três métodos de coleta de amostras bacterianas de estômago de ratos, tanto em uso de placebo quanto em uso de omeprazol. Nota-se uma mudança evidente da microflora bacteriana nos animais em uso de IBPs, sendo melhor identificado pelos métodos de swab e biópsia.

Experimental model in the qualitative and quantitative assessment of non-Helicobacter gastric microflora under proton pump inhibitors action.

PURPOSE: To evaluate models of gastric material collection from Wistar rats with and without using proton pump inhibitors(PPIs). METHODS: Twenty-four rats underwent intraperitoneal omeprazol treatment, and other 12 received similar treatment with 0.9% saline. All animals underwent collection of gastric material samples, after stomach removal, by either biopsies, or aspirates, or swabs. Samples were bacteriologically processed in order to identify species and strains. Values are described as natural logarithm of colony former units per mL [Ln(CFU/mL)]. Kruskal-Wallis and Mann-Whitney non-parametric tests were used, and p<0.05 was set as statistically significant. RESULTS: Significant difference was not seen for Ln (UFC/mL) values among the three methods of collection irrespective of using or not omeprazol. Also, significant difference was not seen in Ln (UFC/mL) values when comparing a method with each others, either using omeprazol or placebo. A significant increase of bacteria strains occurred when PPI was used, and this was seen on the three ways of collection, mainly in biopsy and swab. CONCLUSION: No difference occurred among the three methods of collecting bacteria samples from stomachs of rats, either when using placebo or omeprazol. A remarkable change is seen on animals bacterial microflora when PPIs are used, and bacteria are better identified when swab and biopsy are used.

[Urease test of the gastric content deposits for diagnosis of Helicobacter pylori infection in the gastric mucosa].

A rapid urease test was applied to the examination of the deposit of gastric juice for diagnosing H. pylori in the gastric mucosa. Two hundred and twenty patients blindly randomized were examined in a case control study. The standard rapid urease test kit Jatrox-H.p.-Test (Rohm Pharma, Germany) was used to determine urease activity in the deposit of gastric juice and duodenal [n = 110 (Group 1)] and gastroduodenal [n = 110 (Group 2)] mucosae. Giemsa staining was employed as a comparison method to examine H. pylori infection in the gastric and duodenal mucosae. The availability of regions of duodenal metaplasia was confirmed by periodic acid-Schiff and alcian blue (Serva) staining tests (pH 1.0 and 2.5, respectively). The results of evaluation of the efficiency of the rapid urease test of gastric juice deposit and gastric and duodenal mucosae in Groups 1 and 2 were as follows: sensitivity (SE) (0.97, 0.99, 0,96), specificity (SP) (0.97, 0.97, 0.99), prevalence (0.64, 0.67, 0.24), test accuracy (TA) (0.96, 0.98, 0.98), negative (0.95, 0.97, 0.99) and positive (0.98, 0.99, 0.96) predictive values; positive (38.8, 33.0, 96.0) and negative (0.03, 0.01, 0.04) likelihood ratios. It is expedient to employ the rapid urease test for the diagnosis of H. pylori infection in the stomach (Se 96-99%, Sp 97%, TA 97-98%). When the test of gastric juice deposit and gastric biopsy is positive, the probability of gastric H. pylori availability is 98-99%. When the test is negative (the probability of H. pylori absence is 95-97%), duodenal biopsy is made. When the test of duodenal biopsy is positive, the probability of H. pylori availability is 96%. When it is negative, the probability of H. pylori absence is 99%. An algorithm of use of the rapid urease test to diagnose H. pylori in different intestinal parts (stomach, duodenum) has been developed.

Comparison of biopsy-based methods for the detection of Helicobacter pylori infection.

Various biopsy-based methods for the detection of Helicobacter pylori are evaluated to determine their sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV), followed by polymerase chain reaction (PCR) for the 16S ribosomal RNA (rRNA) gene of H. pylori (16S PCR) to confirm the results. Seventyfive patients (65% [49] males, age range: 17-77 years, mean 42+/-14.6 years) with dyspeptic symptoms are included in the study. Gastric antrum biopsy specimens collected during endoscopy are tested using a urea agar base enriched with 40% urea solution (eUAB, Oxoid)), a commercial rapid urease test (Pronto Dry, Medical Instrument Corp, Switzerland), histopathology and 16S PCR. The eUAB test showed 97% sensitivity, 86% specificity, 84% PPV, 97% NPV and 91% accuracy when the diagnosis of H. pylori infection was made with positive Pronto Dry and histopathology. Pronto Dry showed 100% sensitivity, 82% specificity, 80% PPV, 100% NPV and 89% accuracy when the diagnosis of H. pylori infection was made on positive histopathology and eUAB. Thus, the eUAB can be used as a rapid urease test. It is economical and has a sensitivity and specificity comparable to a commercially available rapid urease test to detect urease activity of H. pylori in gastric biopsy.

[Assessment of selected tests in diagnostics of Helicobacter pylori infections]. / Ocena wybranych testów do rozpoznawania zakazenia Helicobacter pylori.

UNLABELLED: In the diagnostics of Helicobacter pylori infections the invasive and noninvasive methods are applied. In the epidemiological studies the measurement of antibodies of IgG class against H. pylori in the serum or the respiratory test is used. The aim of the study was comparative evaluation of diagnosing of H. pylori infection on the basis of the measurement of antibodies in the serum, HpFL antigens in stool and culture of biopsy specimens from the gastric mucous. MATERIAL AND METHODS: The study included 380 children aged 1-18 years drawn randomly for epidemiological analysis of H. pylori infection in Lower Silesia in the year 2001. The study was conducted in the year 2002. In all children the concentration of antibodies against H. pylon' of IgG class in the serum using the ELISA method as well as H. pylori antigen (HpFL) in stool were determined. In 66 children out of the whole group the measurements of antibodies using ELISA method and immunoblotting as well as HpFL test were compared to the results of H. pylori culture. Additionally the Hp Cag (+) strains were determined. RESULTS: The study demonstrated that in 10% of patients with negative results of IgG class antibodies against H. pylori measurement in the serum (below 24 U/ml) the HpFL test in stool was positive. The sensitivity of the test was 58.9%, specificity 90.0%. The correspondence of HpFL test with positive test for the antibodies in the serum was 90% for the antibodies concentration above 500 U/ml. Assuming that a definite test for the H. pylori infection is culture, the most accurate test for detection of the infection turned out to be the determination of the antigen in the stool and immunoblotting. The parallel increase of antibodies titre together with the increase of prevalence of infection with Hp Cag (+) strains was demonstrated. CONCLUSIONS: The results of HpFL test in stool samples are comparable to the culture, immunoblotting and antibodies concentration in the serum above 100 U/ml.

The effect of Helicobacter pylori eradication in patients with functional dyspepsia: assessment of different diagnostic tests.

BACKGROUND/AIMS: Helicobacter pylori infection, is seen in more than 80% of adult population in Turkey. The aims of this study were 1) to evaluate the importance of the diagnostic tests 2) to investigate the relationship between Hp infection and functional dyspepsia. METHODS: A total 75 patients with functional-dyspepsia were involved into the study. Hp infection was diagnosed by histopathological examination. CLO, cytology, culture, stool antigen and breath test. Symptom score using ROME II criteria was also evaluated to all patients. All patients were taken ranitidine-bismuth-citrate (400mg bid/day), clarithromycin (500 mg bid/day) and amoxicillin (1000 mg bid/day) for 14 days. All tests and symptom score analyses were re-applied at month 1 and 6. RESULTS: The eradication rate was 95.9%. The baseline specifity of breath test, CLO, cytology, culture and stool antigen were 87.3%, 95.4%, 95.4% 94.5% and 86.4%, respectively. The sensitivity of such tests at first month after stopping the treatment were 86.1%, 100%, 100%, 100%, 84.7%, respectively, and were 91.6%, 100%, 100%, 100%, 87.5%, respectively at six months after treatment. Symptom scores were 29.6+/-5.4, 15.8+/-4.7 and 17.9+/-5.3 at baseline, first month and six months after treatment, respectively (p<0.001). CONCLUSIONS: The success of eradication may be related to use of bismuth which prevents antibiotic resistance development. Stool antigen and breath tests are less effective than invasive diagnostic-tests. The finding of improved symptomscores after eradication suggests that Hp may play a role in functional dyspepsia.