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1.  Helicobacter pylori infection 
Clinical Evidence  2009;2009:0406.
The principal effect of Helicobacter pylori infection is lifelong chronic gastritis, affecting up to 20% of younger adults but 50% to 80% of adults born in resource-rich countries before 1950.
Methods and outcomes
We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of H pylori eradication treatment in people with a confirmed duodenal ulcer, a confirmed gastric ulcer, confirmed gastro-oesophageal reflux disease (GORD), confirmed non-ulcer dyspepsia, uninvestigated dyspepsia, localised B cell lymphoma of the stomach, and non-steroidal anti-inflammatory drug (NSAID)-related peptic ulcers? What are the effects of H pylori eradication treatment for preventing NSAID-related peptic ulcers in people with or without previous ulcers or dyspepsia? What are the effects of H pylori eradication treatment on the risk of developing gastric cancer? Do H pylori eradication treatments differ in their effects? We searched: Medline, Embase, The Cochrane Library, and other important databases up to September 2007 (Clinical Evidence reviews are updated periodically; please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).
We found 58 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.
In this systematic review we present information relating to the effectiveness and safety of the following interventions: effects of H pylori eradication in different populations; relative effects of triple regimens, quadruple regimens, and sequential regimens.
Key Points
The principal effect of Helicobacter pylori infection is lifelong chronic gastritis, affecting up to 20% of younger adults but 50% to 80% of adults born before 1950 in resource-rich countries. H pylori infection can be identified indirectly by the C13 urea breath test and stool antigen tests, which are more accurate than serology.Transmission and prevalence rates are higher in areas of childhood poverty. Adult reinfection rates are less than 1% a year.In people with H pylori infection, about 15% will develop a peptic ulcer and 1% will develop gastric cancer during their lifetime.
Eradication of H pylori makes healing of duodenal ulcers more likely and reduces the risk of bleeding with gastric and duodenal ulcers, either alone or when added to antisecretory drug treatment. Eradication also greatly reduces the risk of recurrence of a duodenal ulcer. Eradication reduces recurrence after healing of a gastric ulcer; however, we don't know whether it increases healing of gastric ulcers.Eradication of H pylori may reduce the risk of NSAID-related ulcers in people without previous ulcers; however, we don't know whether it reduces NSAID-related ulcers or bleeding in people with previous ulcers.
In areas of low prevalence of H pylori, few ulcers are caused by H pylori infection. Eradication may be less effective in preventing ulcers in these areas compared with higher-prevalence areas.
Eradication of H pylori reduces symptoms of dyspepsia, but not of GORD. Eradicating H pylori has been shown to reduce dyspeptic symptoms in people with non-ulcer dyspepsia or uninvestigated dyspepsia compared with placebo.
Despite the association between H pylori infection and gastric cancer, no studies have shown a reduced risk after eradication treatment. Gastric B cell lymphoma lesions may regress after H pylori eradication, but we don't know this for sure.
Quadruple and triple regimens seem equally effective at eradicating H pylori as first-line treatments. Quadruple regimens may be more effective as second-line treatment than triple regimens when a first-line triple regimen has failed to eradicate the infection. However, the evidence is limited in that, in comparisons of second-line quadruple versus triple regimens, most triple regimens did not contain a nitroimidazole.
Ten-day sequential therapy may be more effective at eradicating H pylori than a 7-day triple regimen.
Nitroimidazole-based triple regimens and amoxicillin-based triple regimens seem equally effective at eradicating H pylori. High-dose clarithromycin within an amoxicillin-based triple regimen seems more effective at eradicating H pylori than low-dose clarithromycin. However, the dose of clarithromycin within a nitroimidazole-based triple regimen does not seem to have an effect on eradication rates.
Triple regimens using different proton pump inhibitors seem equally effective at eradicating H pylori. Pre-treatment with a proton pump inhibitor before triple regimen does not seem to increase H pylori eradication rates compared with no pre-treatment. Two-week triple proton pump inhibitor regimens may be more effective than 1-week regimens for eradicating H pylori.
Lower eradication rates are achieved in people infected with strains of H pylori that are resistant to antibiotics included in the eradication regimen than are achieved in people infected with sensitive strains of H pylori.
Antibiotics can cause adverse effects such as nausea and diarrhoea. Bismuth may turn the stools black.
PMCID: PMC2907775  PMID: 21718575
2.  Role of Helicobacter pylori in ulcer healing and recurrence of gastric and duodenal ulcers in longterm NSAID users. Response to omeprazole dual therapy. 
Gut  1996;39(1):22-26.
BACKGROUND: The relation between Helicobacter pylori infection and non-steroidal anti-inflammatory drug (NSAID)-associated peptic ulcers remains unclear; in particular, it is not known whether H pylori plays a part in the healing and recurrence of these ulcers. AIMS: To evaluate prospectively in a consecutive series of arthritis patients receiving longterm NSAID treatment the prevalence of peptic ulcer as well as the effect of H pylori eradication on the healing and recurrence of gastric and duodenal ulcer found. PATIENTS: Some 278 consecutive patients underwent gastroscopy with multiple biopsies of the gastric antrum and corpus for histological examination and rapid urease test. One hundred peptic ulcers (59 gastric ulcers, 39 duodenal ulcers, and two gastric ulcers concomitant with a duodenal ulcer) were found. Seventy per cent of these ulcers were H pylori positive. METHODS: According to their H pylori status, ulcer patients were randomised to one of the following treatments: H pylori negative ulcers received omeprazole 20 mg twice daily for four to eight weeks, whereas H pylori positive lesions were treated with omeprazole 20 mg twice daily plus amoxycillin 1 g twice daily (the second of these for the first two weeks) or omeprazole alone for four to eight weeks while continuing NSAID therapy. Patients with healed ulcers were endoscopically followed up for six months after stopping antiulcer therapy while continuing NSAIDs. RESULTS: Endoscopic healing rates for gastric and duodenal ulcers in the three different groups were similar both at four and eight weeks. H pylori eradication did not influence healing, which occurred in 14 of 20 (70%) of patients in whom H pylori was eradicated, compared with 14 of 17 (82%) of patients with persistent infection. Cumulative recurrence rates at six months did not statistically differ among the three different groups (27% in H pylori negative, 46% in H pylori positive, and 31% in those where H pylori was eradicated during the healing phase), although a numerical trend in favour of a higher recurrence rate in infected patients was evident. CONCLUSIONS: H pylori eradication does not confer any significant advantage on the healing of gastric and duodenal ulcers associated with longterm NSAID use. It remains to be established with certainty whether eradication may be helpful in the reduction of recurrence in a specific subset of NSAID associated ulcer.
PMCID: PMC1383224  PMID: 8881802
3.  Serological Assessment of the Early Response to Eradication Therapy Using an Immunodominant Outer Membrane Protein of Helicobacter pylori 
Eradication of Helicobacter pylori infection cures gastritis and prevents recurrence of peptic ulcers. Endoscopy is usually used to evaluate the effectiveness of eradication therapy. We designed a new noninvasive assay system for the early evaluation of eradication of H. pylori infection in which a crude H. pylori outer membrane protein preparation (HPOmp) is used as an antigen, and we determined the sensitivity and specificity of the serological assay system. Immunoblot analysis showed that anti-HPOmp antibodies reacted to a protein with a molecular mass of approximately 29 kDa. In those patients who responded to therapy, the anti-HPOmp immunoglobulin G (IgG) titers measured by enzyme-linked immunosorbent assay (ELISA) at 1 month after the end of therapy were significantly lower than those before treatment (34.8% reduction; P < 0.001), and the posttreatment reduction in the antibody titer was significantly greater than that of the titer measured with a commercially available anti-H. pylori IgG ELISA (34.8% versus 16.1%; P < 0.001). When a 25% reduction of anti-HPOmp IgG titer at 1 month after the end of treatment was taken as the cutoff value for H. pylori eradication, the sensitivity and specificity of our new assay were 75% (51 of 68 treatment responders) and 96% (22 of 23 nonresponders), respectively. Our results indicate that the novel serological test with HPOmp might be a clinically useful tool for assessment of eradication of H. pylori.
PMCID: PMC96215  PMID: 9801348
4.  The role of screening for Helicobacter pylori in patients with duodenal ulceration in the primary health care setting. 
BACKGROUND: It is known that at least 90% of duodenal ulcers are caused by infection with the bacterium Helicobacter pylori. Eradicating this organism usually results in complete resolution of the disease. Testing for H pylori was introduced relatively recently, and thus, many patients known to have uncomplicated peptic ulcer disease who continue to need long-term treatment with ulcer-healing drugs have never been tested for the infection or offered eradication therapy. In modern computerized practices, this subgroup of patients can readily be identified by reference to morbidity and repeat prescribing data. Eradication of H pylori infection in this group of patients has great potential benefit for the individuals concerned as well as cost-saving benefit for the National Health Service. AIM: The aim of this prospective study was to determine whether it is worthwhile screening for and treating H pylori infection in patients in a general practice population with previously diagnosed duodenal ulcer disease taking ulcer-healing drugs long term. METHOD: In 1994, in a practice of 7100 patients, morbidity and repeat prescribing data were used to identify 40 patients (0.6%) with proven duodenal ulcer disease taking ulcer-healing medication long term and with uncertain H pylori status. Twenty-nine of the 40 subjects agreed to undergo serology testing for H pylori antibodies. Of 20 (69%) who were positive, 18 (eight women, median age 63.8 years) were given eradication therapy. Seventeen patients received omeprazole 40 mg once daily and amoxycillin 500 mg three times daily for 14 days with metronidazole 400 mg three times daily for the first 7 days; for the remaining patient metronidazole was inadvertently omitted. [13C]Urea breath testing was carried out at the local hospital at least one month after therapy to determine whether eradication treatment had been successful. Subjects were also personally followed up by telephone after 1 and 4 months to assess the success of treatment subjectively. RESULTS: [13C]Urea breath testing showed that H pylori eradication was successful in all 17 patients (100%) who received the intended eradication regimen. Helicobacter pylori was not eradicated in the patient who received only omeprazole and amoxycillin. Four months after successful H pylori eradication, 13 of the 17 (76%) patients remained completely asymptomatic. Two of the four patients who had some recurrent dyspepsia had known gastro-oesophageal reflux and their ongoing symptoms after eradication therapy seemed, on close questioning, to be more attributable to this than to duodenal ulcer disease. CONCLUSION: Testing for and eradication of H pylori is worthwhile in general practice in those patients with previous proven duodenal ulceration who need long-term ulcer-healing medication. The high rate of eradication of H pylori achieved with the regimen used in this study compares very favourably with that of other treatment regimens. However, in patients with duodenal ulcers there may be coexisting pathology, and H pylori eradication does not necessarily result in complete disappearance of dyspeptic symptoms. Thus, when monitoring the outcome of treatment it is important to assess improvement of symptoms as well as objective evidence of eradication.
PMCID: PMC1239580  PMID: 8731626
5.  Short-Term Follow-Up by Serology of Patients Given Antibiotic Treatment for Helicobacter pylori Infection 
Journal of Clinical Microbiology  1998;36(5):1193-1196.
Helicobacter pylori serology and in particular enzyme-linked immunosorbent assays for the measurement of immunoglobulin G (IgG) antibody titers form an accurate means of diagnosing H. pylori infection in patients before treatment. H. pylori serology is of limited value in monitoring treatment because of the slow decline in antibody titers. In the present study we aimed to measure the most suitable moment after antibiotic treatment at which serology should be used to monitor treatment. Sixty-four patients who had nonulcer dyspepsia and H. pylori infection and who underwent upper gastrointestinal endoscopy because of persistent dyspeptic symptoms were included in the study. H. pylori cure was confirmed by histology and culture 5 weeks after the completion of the antibiotic treatment. Serological examination was performed before therapy and at 5 weeks, 10 weeks, and 1 year after the completion of antibiotic treatment. Diagnostic performance was assessed by receiver-operating characteristic analysis. The areas under the receiver-operating characteristic curves of the H. pylori antibody titers at 5 weeks, 10 weeks, and 1 year after the completion of treatment were 0.53 (95% confidence interval [CI], 0.36 to 0.69), 0.60 (95% CI, 0.43 to 0.76), and 0.78 (95% CI, 0.63 to 0.93), respectively. The areas under the receiver-operating characteristic curves of the changes in H. pylori IgG antibody titers at 5 weeks, 10 weeks, and 1 year after the completion of treatment in comparison with the pretreatment titers were 0.85 (95% CI, 0.72 to 0.97), 0.96 (95% CI, 0.89 to 1.0), and 1.0 (95% CI, not estimable), respectively. We conclude that serology forms a useful means of monitoring treatment in patients with nonulcer dyspepsia and H. pylori infection as early as 10 weeks and maybe even sooner after the completion of treatment for the infection.
PMCID: PMC104798  PMID: 9574675
6.  Effect of Helicobacter pylori eradication on chronic gastritis during omeprazole therapy 
Gut  2000;46(5):615-621.
BACKGROUND—We have previously observed that profound acid suppressive therapy in Helicobacter pylori positive patients with gastro-oesophageal reflux disease is associated with increased corpus inflammation and accelerated development of atrophic gastritis.
AIM—To investigate if H pylori eradication at the start of acid suppressive therapy prevents the development of these histological changes.
PATIENTS/METHODS—In a prospective randomised case control study, patients with reflux oesophagitis were treated with omeprazole 40 mg once daily for 12 months. H pylori positive patients were randomised to additional double blind treatment with omeprazole 20 mg, amoxicillin 1000 mg and clarithromycin 500 mg twice daily or placebo for one week. Biopsy sampling for histology, scored according to the updated Sydney classification, and culture were performed at baseline, and at three and 12 months.
RESULTS—In the persistently H pylori positive group (n=24), active inflammation increased in the corpus and decreased in the antrum during therapy (p=0.032 and p=0.002, respectively). In contrast, in the H pylori positive group that became H pylori negative as a result of treatment (n=33), active and chronic inflammation in both the corpus and antrum decreased (p⩽0.0001). The decrease in active and chronic inflammation in the corpus differed significantly compared with the persistently H pylori positive group (both p=0.001). For atrophy scores, no significant differences were observed between H pylori eradicated and persistently H pylori positive patients within one year of follow up. No changes were observed in the H pylori negative control group (n=26).
CONCLUSIONS—H pylori eradication prevents the increase in corpus gastritis associated with profound acid suppressive therapy. Longer follow up is needed to determine if H pylori eradication prevents the development of atrophic gastritis.

Keywords: Helicobacter pylori; gastritis; omeprazole; atropy; gastro-oesophageal reflux disease
PMCID: PMC1727929  PMID: 10764703
7.  Capsaicin-sensitive afferentation represents an indifferent defensive pathway from eradication in patients with H. pylori gastritis 
AIM: To study the role of capsaicin-sensitive afferent nerves in Helicobacter pylori (H. pylori) positive chronic gastritis before and after eradication.
METHODS: Gastric biopsy samples were obtained from corpus and antrum mucosa of 20 healthy human subjects and 18 patients with H. pylori positive chronic gastritis (n = 18) before and after eradication. Traditional gastric mucosal histology (and Warthin-Starry silver impregnation) and special histochemical examinations were carried out. Immunohistochemistry for capsaicin receptor (TRVP1), calcitonin gene-related peptide (CGRP) and substance P (SP) were carried out by the labeled polymer immunohistological method (Lab Vision Co., USA) using polyclonal rabbit and rat monoclonal antibodies (Abcam Ltd., UK).
RESULTS: Eradication treatment was successful in 16 patients (89%). Seven patients (7/18, 39%) remained with moderate complaints, meanwhile 11 patients (11/28, 61%) had no complaints. At histological evaluation, normal gastric mucosa was detected in 4 patients after eradication treatment (4/18, 22%), and moderate chronic gastritis could be seen in 14 (14/18, 78%) patients. Positive immuno-staining for capsaicin receptor was seen in 35% (7/20) of controls, 89% (16/18, P < 0.001) in patients before and 72% (13/18, P < 0.03) after eradication. CGRP was positive in 40% (8/20) of controls, and in 100% (18/18, P < 0.001) of patients before and in 100% (18/18, P < 0.001) after eradication. The immune-staining of gastric mucosa for substance-P was positive in 25% (5/20) of healthy controls, and in 5.5% (3/18, P > 0.05) of patients before and in 0% of patients (0/18, P > 0.05) after H. pylori eradication.
CONCLUSION: Distibution of TRVP1 and CGRP is altered during the development of H. pylori positive chronic gastritis. The immune-staining for TRVP1, CGRP and SP rwemained unchanged before and after H. pylori eradication treatment. The capsaicin-sensitive afferentation is an independent from the eradication treatment. The 6 wk time period might not be enough time for the restituion of chronic H. pylori positive chronic gastritis. The H. pylori infection might not represent the main pathological factor in the development of chronic gastritis
PMCID: PMC3205120  PMID: 22046579
Capsaicin-sensitive afferentation; Helicobacter pylori; Eradication therapy; Afferent and efferent vagal nerves; Transient potential vanilloid receptor 1; Calcitonin gene-related peptide; Substance P
8.  Efficacy of omeprazole and amoxicillin with either clarithromycin or metronidazole on eradication of Helicobacter pylori in Chinese peptic ulcer patients 
AIM: One-week triple therapy with proton pump inhibitors, clarithromycin and amoxicillin has recently been proposed as the first-line treatment for Helicobacter pylori (H pylori) infection; however, data regarding the effects of this regimen in China are scarce. The aim of this prospective and randomized study was to compare the efficacy of clarithromycin and metronidazole when they were combined with omeprazole and amoxicillin on eradication of H pylori and ulcer healing in Chinese peptic ulcer patients.
METHODS: A total of 103 subjects with H pylori-positive peptic ulcer were randomly divided into two groups, and accepted triple therapy with omeprazole 20 mg, amoxicillin 1000 mg and either clarithromycin 500 mg (OAC group, n = 58) or metronidazole 400 mg (OAM group, n = 45). All drugs were given twice daily for 7 d. Patients with active peptic ulcer were treated with omeprazole 20 mg daily for 2-4 wk after anti-H pylori therapy. Six to eight weeks after omeprazole therapy, all patients underwent endoscopies and four biopsies (two from the antrum and two others from the corpus of stomach) were taken for rapid urease test and histological analysis (with modified Giemsa staining) to examine H pylori. Successful eradication was defined as negative results from both examination methods.
RESULTS: One hundred patients completed the entire course of therapy and returned for follow-up. The eradication rate of H pylori for the per-protocol analysis was 89.3% (50/56) in OAC group and 84.1% (37/44) in OAM group. Based on the intention-to-treat analysis, the eradication rate of H pylori was 86.2% (50/58) in OAC group and 82.2% (37/45) in OAM group. There were no significant differences in eradication rates between the two groups on either analysis. The active ulcer-healing rate was 96.7% (29/30) in OAC group and 100% (21/21) in OAM group (per-protocol analysis, P>0.05). Six patients in OAC group (10.3%) and five in OAM group (11.1%) reported adverse events (P>0.05).
CONCLUSION: One-week triple therapy with omeprazole and amoxicillin in combination with either clarithromycin or metronidazole is effective for the eradication of H pylori. The therapeutic regimen comprising metronidazole with low cost, good compliance and mild adverse events may offer a good choice for the treatment of peptic ulcers associated with H pylori infection in China.
PMCID: PMC4305638  PMID: 15832421
Omeprazole; Amoxicillin; H pylori
9.  Differential Normalization of Mucosal Interleukin-8 and Interleukin-6 Activity after Helicobacter pylori Eradication 
Infection and Immunity  1998;66(10):4742-4747.
There is differential resolution of mucosal infiltration with neutrophils and mononuclear cells following successful Helicobacter pylori eradication. We investigated the effects of H. pylori eradication on mucosal interleukin-8 (IL-8) and IL-6 activity in relation to the resolution of H. pylori-associated gastritis. Eighty-one duodenal ulcer patients with H. pylori infection received dual- or triple-treatment eradication therapy, and mucosal biopsy specimens obtained at the initial and follow-up endoscopic examinations were cultured in vitro for 24 h. The levels of IL-8 and IL-6 were measured by enzyme-linked immunosorbent assays. In the 42 patients in whom H. pylori eradication failed, there was little change in the numbers of neutrophils and mononuclear cells infiltrating the mucosa and in IL-8 and IL-6 activity. In the 39 patients in whom H. pylori was eradicated, there was normalization both in the numbers of infiltrating neutrophils and in mucosal IL-8 activity, which was evident within 1 month following therapy. In contrast, there was a gradual resolution of mononuclear cell infiltration over a 6-month period, accompanied by a gradual normalization in IL-6 levels. Addition of H. pylori to cultures of mucosal tissues induced a significant increase in IL-8 activity in both uninfected control subjects and patients from whom H. pylori was eradicated. However, this introduction yielded a significant increase in IL-6 activity only in the latter group. This study indicates a dichotomy in the changes of mucosal IL-8 and IL-6 activity after H. pylori eradication. The rapid normalization of IL-8 after H. pylori eradication and the ability of H. pylori cells to stimulate IL-8 in control tissues indicate that IL-8 induction is a part of the innate (nonimmune) responses to this organism. In contrast, the results of experiments analyzing IL-6 activity in cultured mucosal tissues suggest that the gradual resolution of mucosal IL-6 activity and mononuclear infiltration after successful eradication observed in vivo may reflect gradually diminishing residual immune responses against H. pylori.
PMCID: PMC108584  PMID: 9746573
10.  CagA and VacA Helicobacter pylori antibodies in gastric cancer 
Infection with different genotypes of virulent Helicobacter pylori strains (cytotoxin-associated gene A [CagA]-and/or vacuolating cytotoxin A [VacA]-positive) can play a role in the development of atrophic gastritis, duodenal ulcer (DU) and gastric cancer (GC).
To determine whether patients with GC and H pylori-negative histological staining had previously been infected with H pylori CagA- and/or VacA-positive virulent strains.
Twenty-three GC patients with a mean (± SD) age of 68.14±9.8 years who tested H pylori-negative on histological staining took part in the study. Three control groups were included. The first group comprised 19 patients with past H pylori infection and DUs eradicated 10 years earlier, with a mean age of 58±18.2 years. H pylori-negative status for this group was determined every year with Giemsa staining, and follow-up testing occured 120±32 months (mean ± SD) after therapy. The subsequent control groups included 20 asymptomatic children, with a mean age of 7±4.47 years, and with H pylori-negative fecal tests; the final group contained 30 patients without clinical symptoms of H pylori infection, with a mean age of 68±11.6 years, who tested H pylori-negative by histological staining.
Prevalence of CagA and VacA seropositivity, respectively was 82.6% and 73.91% in GC patients; 84.2% and 84.2% in H pylori-negative DU patients; 25% and 5% in H pylori-negative children; and 36.6% and 16.6% in the patients without clinical symptoms on histological staining. CagA and VacA antibody positivity was not significantly different between GC patients and patients with DUs that had been eradicated 10 years earlier. Significant positivity was found between the children’s group and the H pylori-negative (with past DUs) group (P<0.001). A statistically significant difference was found in age between groups (P<0.03).
Patients with GC, even when H pylori-negative at the time of the present study, may have been infected by H pylori before the onset of the disease, as confirmed by CagA and VacA seropositivity. These data reinforce the hypothesis that H pylori may be a direct carcinogenic agent of GC.
PMCID: PMC2662200  PMID: 18354754
CagA; Gastric cancer; Helicobacter pylori; VacA
11.  Evaluation of Pyloriset Screen, a Rapid Whole-Blood Diagnostic Test for Helicobacter pylori Infection 
Journal of Clinical Microbiology  1998;36(4):955-957.
Helicobacter pylori infection can be detected by several invasive tests based on gastroscopy and by noninvasive methods such as serologic assays. Noninvasive tests can be used not only in addition to invasive tests but also by themselves to screen for H. pylori infection in patients who are not in urgent need of endoscopy. Lately, rapid qualitative serologic tests have been developed. In the present study, the accuracy of a novel rapid whole-blood test, Pyloriset Screen, detecting immunoglobulin G (IgG) and IgA antibodies against H. pylori was evaluated. A total of 207 consecutive adult outpatients referred for upper endoscopy were enrolled. Gastric biopsy specimens were taken from the antrum and corpus for histologic examination and rapid urease testing. Cultures were available for 113 patients. Serum samples collected from all patients were tested for H. pylori antibodies by two enzyme immunoassays (EIAs) (Pyloriset EIA and an in-house EIA), a rapid latex agglutination test (Pyloriset Dry), and Pyloriset Screen. Patients were considered H. pylori positive if helicobacters were seen on histologic examination (77 patients) or, if in combination with histologically verified (although helicobacter-negative) gastritis, their IgG antibody titers were elevated in the two EIAs (five patients). The Pyloriset Screen test had a sensitivity of 95%, a specificity of 94%, a positive predictive value of 91%, and a negative predictive value of 97%. Among 63 patients under the age of 45 years, the Pyloriset Screen test did not miss a single H. pylori diagnosis, and only 1 patient had a false-positive result. Pyloriset Screen could be used reliably to screen for H. pylori infection.
PMCID: PMC104667  PMID: 9542915
12.  CagA Antibodies in Japanese Children with Nodular Gastritis or Peptic Ulcer Disease 
cagA+ Helicobacter pylori strains have been linked to more severe gastric inflammation, peptic ulcer disease, and gastric cancer in adults, but there have been few studies of cagA in children. We examined the relationship between H. pylori cagA status and clinical status in Japanese children. Forty H. pylori-positive children were studied: 15 with nodular gastritis, 5 with gastric ulcers, and 20 with duodenal ulcers. H. pylori status was confirmed by biopsy-based tests and serum anti-H. pylori immunoglobulin G (IgG) antibody. As controls, 77 asymptomatic children with sera positive for anti-H. pylori IgG were enrolled. Levels of IgG antibodies to CagA in serum were measured by an antigen-specific enzyme-linked immunosorbent assay. In 16 patients with successful H. pylori eradication, posttreatment levels of CagA and H. pylori IgG antibodies also were studied. The CagA antibody seropositivities of asymptomatic controls (81.8%) and patients with nodular gastritis, gastric ulcers, and duodenal ulcers (80.0 to 95.0%) were not significantly different. Compared with pretreatment levels of CagA antibodies, posttreatment levels decreased progressively and significantly. We conclude that, as in Japanese adults, a high prevalence of cagA+ H. pylori strains was found in Japanese children, and that there was no association with nodular gastritis or peptic ulcer disease. In the assessment of eradicative therapies, monitoring of serum anti-CagA antibodies does not appear to offer any direct benefit over monitoring of anti-H. pylori antibodies.
PMCID: PMC86021  PMID: 10618065
13.  Effects of Helicobacter pylori eradication on the natural history of lymphocytic gastritis 
Gut  1999;45(4):495-498.
BACKGROUND—Lymphocytic gastritis is characterised by an accumulation of lymphocytes in the surface epithelium of the stomach. Lymphocytic gastritis has been linked to coeliac disease and Helicobacter pylori infection.
AIMS—To determine whether H pylori eradication leads to resolution of the lymphocytic infiltrate and clinical improvement in patients with lymphocytic gastritis, and to determine their HLA status.
METHODS—The Leeds Dyspepsia Questionnaire (LDQ) was administered to 13 patients with lymphocytic gastritis. H pylori serology, 13C urea breath test (UBT), and upper gastrointestinal endoscopy with sampling of the duodenum, antrum, and corpus were done in all cases and the HLA status was determined. Eleven patients had at least one positive test for H pylori. Patients with lymphocytic gastritis and H pylori infection were treated with a one week course of omeprazole, clarithromycin, and metronidazole. Gastric and duodenal intraepithelial lymphocyte (IEL) counts were performed, along with histological assessment of gastric and duodenal biopsies before and after H pylori eradication.
RESULTS—Two months after treatment there was a significant reduction in gastric IEL counts in both antrum and corpus. There was no significant change in duodenal IEL counts before and after eradication. According to the Sydney grading there was significant improvement in corpus inflammation after eradication. The patients histologically H pylori positive before treatment became H pylori negative. Dyspepsia scores also improved significantly after treatment.
CONCLUSIONS—H pylori eradication treatment in patients with lymphocytic gastritis causes significant improvement in the gastric IEL infiltrate, corpus inflammation, and dyspeptic symptoms. H pylori serology is frequently positive when histology and UBT are negative. Lymphocytic gastritis may represent a specific immune response to H pylori infection.

Keywords: lymphocytic gastritis; intraepithelial lymphocytes; Helicobacter pylori; HLA status; coeliac disease
PMCID: PMC1727676  PMID: 10486354
14.  Atrophic gastritis and Helicobacter pylori infection in outpatients referred for gastroscopy 
Gut  2000;46(4):460-463.
BACKGROUND—Atrophic gastritis has been shown to be one of the long term sequelae of Helicobacter pylori infection.
AIMS—To determine the prevalence of atrophic gastritis in outpatients, to study the accuracy of serological methods for revealing atrophy, and to define the association of H pylori infection with atrophic gastritis in these patients.
PATIENTS/METHODS—A total of 207 consecutive outpatients referred for gastroscopy were included. Biopsy specimens from the antrum and corpus were assessed histologically according to the Sydney system. Serum samples were studied for H pylori IgG and IgA antibodies by enzyme immunoassay, CagA antibodies by immunoblot, pepsinogen I by an immunoenzymometric assay, gastrin by radioimmunoassay, and parietal cell antibodies by indirect immunofluorescence.
RESULTS—Histological examination revealed atrophic gastritis in 52 (25%) of 207 patients. H pylori and CagA antibodies were strongly associated with atrophic antral gastritis but poorly associated with atrophic corpus gastritis. Low serum pepsinogen I was the most sensitive and specific indicator of moderate and severe atrophic corpus gastritis. All six patients with moderate atrophic corpus gastritis had H pylori infection but eight of 10 patients with severe atrophic corpus had increased parietal cell antibodies and nine had no signs of H pylori infection.
CONCLUSIONS—Atrophic antral gastritis was strongly associated with CagA positive H pylori infection. Severe atrophic corpus gastritis was not determined by H pylori tests but low serum pepsinogen I, high gastrin, and parietal cell antibodies may be valuable in detecting these changes.

Keywords: Helicobacter pylori; atrophic gastritis; CagA antibodies; Helicobacter pylori antibodies; pepsinogen; parietal cell antibodies
PMCID: PMC1727900  PMID: 10716672
15.  Patients with established gastro-esophageal reflux disease might benefit from Helicobacter pylori eradication 
The aim of this study was to investigate the effect of Helicobacter pylori (H. pylori) eradication in selected H. pylori-positive patients with a primary diagnosis of gastro-esophageal reflux disease (GERD) by using the 3-h postprandial esophageal pH monitoring.
We recruited patients with erosive esophagitis at endoscopy and H. pylori infection at histology, successfully cured following eradication therapy; the selected H. pylori-positive patients had weekly reflux symptoms for at least six months and endoscopically established Grade A or B esophagitis. Twenty-nine eligible patients were initially subjected to esophageal manometry and ambulatory 3-h postprandial esophageal pH monitoring. All patients received H. pylori triple eradication therapy accompanied by successful H. pylori eradication. After successful eradication of H. pylori (confirmed by 13C urea breath test), a second manometry and 3-h postprandial esophageal pH monitoring were introduced to assess the results of eradication therapy, after a 3-month post-treatment period.
All 29 selected H. pylori-positive patients became negative due to successful H. pylori eradication, evaluated by 13C urea breath test after a 4-week post-treatment period. Post-eradication, 62.1% patients showed similar manometric pattern at baseline; 17.2% showed improvement; 17.2% normalization; and 3.4% deterioration of the manometric patterns. The DeMeester symptom scoring in the 3-h postprandial ambulatory esophageal pH monitoring was improved after eradication of H. pylori (median 47.47 vs. 22.00, Wilcoxon’s singed rank; P=0.016). On comparing the pH monitoring studies for each patient at baseline and post-eradication period, 82.8% patients showed improvement and 17.2% deterioration of the DeMeester score.
By using 3-h postprandial esophageal pH monitoring, this study showed, for the first time, that H. pylori eradication may positively influence GERD symptoms. Large-scale controlled relative studies are warranted to confirm these findings.
PMCID: PMC4188932  PMID: 25330805
Helicobacter pylori; gastro-esophageal reflux disease; esophageal pH monitoring; DeMeester symptom scoring
16.  Efficacy of serology driven “test and treat strategy” for eradication of H. pylori in patients with rheumatic disease in the Netherlands 
The treatment of choice of H. pylori infections is a 7-day triple-therapy with a proton pump inhibitor (PPI) plus amoxicillin and either clarithromycin or metronidazole, depending on local antibiotic resistance rates. The data on efficacy of eradication therapy in a group of rheumatology patients on long-term NSAID therapy are reported here. This study was part of a nationwide, multicenter RCT that took place in 2000–2002 in the Netherlands. Patients who tested positive for H. pylori IgG antibodies were included and randomly assigned to either eradication PPI-triple therapy or placebo. After completion, follow-up at 3 months was done by endoscopy and biopsies were sent for culture and histology. In the eradication group 13% (20/152, 95% CI 9–20%) and in the placebo group 79% (123/155, 95% CI 72–85%) of the patients were H. pylori positive by histology or culture. H. pylori was successfully eradicated in 91% of the patients who were fully compliant to therapy, compared to 50% of those who were not (difference of 41%; 95% CI 18–63%). Resistance percentages found in isolates of the placebo group were: 4% to clarithromycin, 19% to metronidazole, 1% to amoxicillin and 2% to tetracycline.
PMCID: PMC3104134  PMID: 21293900
17.  Effect of Helicobacter pylori Eradication According to the IL-8-251 Polymorphism in Koreans 
Journal of Korean Medical Science  2012;27(10):1202-1207.
Previous studies suggested that polymorphisms of proinflammatory cytokine genes are important host genetic factors in Helicobacter pylori infection. The present study evaluated whether IL-8-251 polymorphism affected H. pylori eradication rate and to investigate the effect of H. pylori eradication on angiogenesis and the inflammatory process according to the IL-8-251 polymorphism. A total of 250 H. pylori-positive patients treated by endoscopic resection of the gastric neoplasm were classified into 3 groups (134 H. pylori-eradicated group, 19 H. pylori-eradication failure group, and 97 H. pylori-infected group). H. pylori status, histology, and angiogenic factor levels were evaluated at baseline, 6 months, and 18 months. H. pylori eradication rate was 92.9% in AA genotype, 85.7% in AT genotype and 88.4% in TT genotype (P value = 0.731). Elevated IL-8 and matrix metalloproteinase-9 concentrations in H. pylori-infected gastric mucosa were reversible by successful eradication of H. pylori, independent of the IL-8-251 polymorphism. It is suggested that elevated IL-8 and MMP-9 concentrations in H. pylori-infected gastric mucosa are altered significantly after successful eradication and these conditions continue for 18 months. However, IL-8-251 polymorphism does not affect H. pylori eradication rate and the sequential changes of related angiogenic factors after H. pylori eradication in Koreans.
PMCID: PMC3468757  PMID: 23091318
Helicobacter pylori; Interleukin-8; Polymorphism
18.  Efficacy and cost-effectiveness of the 13C-urea breath test as the primary diagnostic investigation for the detection of Helicobacter pylori infection compared to invasive and non-invasive diagnostic tests 
Helicobacter pylori (H. pylori) is one of the most common bacterial infections in humans. There is a risk factor for gastric or duodenal ulcers, gastric cancer and MALT (Mucosa Associated Lymphoid Tissue)-Lymphomas. There are several invasive and non-invasive methods available for the diagnosis of H. pylori. The 13C-urea breath test is a non-invasive method recommended for monitoring H. pylori eradication therapy. However, this test is not yet used for primary assessment of H. pylori in Germany.
What are the clinical and health economic benefits of the 13C-urea breath test in the primary assessment of H. pylori compared to other invasive and non-invasive methods?
A systematic literature search including a hand search was performed for studies investigating test criteria and cost-effectiveness of the 13C-urea breath test in comparison to other methods used in the primary assessment of H. pylori. Only studies that directly compared the 13C-urea breath test to other H. pylori-tests were included. For the medical part, biopsy-based tests were used as the gold standard.
30 medical studies are included. Compared to the immunoglobulin G (IgG) test, the sensitivity of the 13C-urea breath test is higher in twelve studies, lower in six studies and one study reports no differences. The specificity is higher in 13 studies, lower in three studies and two studies report no differences. Compared to the stool antigen test, the sensitivity of the 13C-urea breath test is higher in nine studies, lower in three studies and one study reports no difference. The specificity is higher in nine studies, lower in two studies and two studies report no differences. Compared to the urease test, the sensitivity of the 13C-urea breath test is higher in four studies, lower in three studies and four studies report no differences. The specificity is higher in five studies, lower in five studies and one study reports no difference. Compared to histology, the sensitivity of the 13C-urea breath test is higher in one study and lower in two studies. The specificity is higher in two studies and lower in one study. One study each compares the 13C-urea breath test to the 14C-urea breath test and the polymerase chain reaction (PCR) test, respectively, and reports no difference in sensitivity and specificity with the 14C-urea breath test, and lower sensitivity and higher specificity compared to PCR. The statistical significance of these differences is described for six of the 30 studies.
Nine health economic evaluations are included in the Health Technology Assessment (HTA) report. Among these studies, the test-and-treat strategy using the 13C-urea breath test is compared to test-and-treat using serology in six analyses and to test and treat using the stool antigen test in three analyses. Thereby, test-and-treat using the breath test is shown to be cost-effective over the serology based strategy in three models and is dominated by a test-and-treat strategy using the stool antigen test in one model. A cost-effectiveness comparison between the urea breath test approach and the empirical antisecretory therapy is carried out in four studies. Of these, two studies report that the strategy using the urea breath test is cost-effective over the empirical antisecretory therapy. In two studies, test-and-treat using the 13C-urea breath test is compared to the empirical eradication therapy and in five studies to endoscopy-based strategies. The breath test approach dominates endoscopy in two studies and is dominated by this strategy in one study.
All included medical and economic studies are limited to a greater or lesser extent. Additionally, the results of the studies are heterogeneous regarding medical and economic outcomes respectively. Thus, the majority of the medical studies do not report the statistical significance of the differences in sensitivity and specificity. In direct comparisons the 13C- urea breath test shows higher sensitivity and specificity than the IgG and stool antigen tests. In comparison to the urease test, results for sensitivity are inconsistent, and the specificity is slightly higher for the 13C-urea breath test. There are not enough results for comparisons between the 13C-urea breath test and the 14C-urea breath test, histology and PCR to describe tendencies.
The included economic studies suggest that the test-and-treat strategy using the 13C-urea breath test is cost-effective compared to test-and-treat using serology as well as empirical antisecretory therapies. Due to a lack of valid studies, it is not possible to assess the breath test approach in comparison to test-and-treat using the stool antigen test and the empirical eradication therapy respectively, regarding the cost-effectiveness. The results of economic analyses comparing test-and-treat using the breath test to endoscopy strategies are too heterogeneous to draw any conclusions. Overall, none of the included economic models is able to completely capture the complexity of managing patients with dyspeptic complaints.
Based on available medical and economic studies, there is no sufficient evidence to recommend test and-treat using 13C-urea breath testing for the detection of H. pylori infection as the standard procedure for the management of uninvestigated dyspepsia in the German health care system. In addition, it must be considered that the DVGS guidelines of the Deutsche Gesellschaft für Verdauungs- und Stoffwechselkrankheiten (DVGS) recommend endoscopy based methods for the management of patients with dyspeptic complaints.
PMCID: PMC3011289  PMID: 21289901
19.  Effect of Helicobacter pylori eradication on serum ghrelin and obestatin levels 
AIM: To investigate changes in serum ghrelin and obestatin levels before and after Helicobacter pylori (H. pylori) eradication.
METHODS: A total of 92 patients presenting with symptoms of dyspepsia were enrolled in the study. Upper endoscopy was performed on all patients and used to diagnose H. pylori infection according to the presence of characteristic histopathological findings; seventy patients were diagnosed with H. pylori infection and the remaining 22 non-infected patients were classified as healthy controls. H. pylori eradication was accomplished by administering the classical triple therapy drug regimen, consisting of lansoprazole 30 mg bid, amoxicillin 1 g bid, and clarithromycin 500 mg tid for 14 d. The eradication of H. pylori was assessed with C14-urea breath test, which was performed at eight weeks after treatment. Levels of serum active ghrelin and obestatin were assessed at beginning of the study (prior to treatment) and after eight weeks. The levels were comparatively analyzed between the H. pylori negative control group, the H. pylori eradicated group, and the H. pylori non-eradicated group.
RESULTS: A total of 92 patients, 50 females and 42 males with a mean age of 38.2 ± 11.9 years (range: 19-64), were analyzed. H. pylori eradication success was achieved in 74.3% (52/70) of H. pylori positive patients. The initial levels of ghrelin in the H. pylori positive and control cases were 63.6 ± 19.8 pg/mL and 65.1 ± 19.2 pg/mL (P = 0.78), respectively, and initial obestatin levels were 771 ± 427 pg/mL and 830 ± 296 pg/mL (P = 0.19), respectively. The difference between the initial levels and the week 8 levels of ghrelin and obestatin in the control group was insignificant [4.5% (P = 0.30) and -0.9% (P = 0.65), respectively]. The difference between the initial and week 8 levels of ghrelin and obestatin in the H. pylori non-eradicated group were also insignificant [0.9% (P = 0.64) and 5.3% (P = 0.32), respectively]. The H. pylori eradicated group had a greater change in obestatin levels when compared to the control and the non-eradicated groups (148 ± 381 pg/mL vs -12 ± 138 pg/mL and -72.8 ± 203 pg/mL, respectively, P = 0.015), while decreases in ghrelin levels were insignificant (-7.2 pg/mL vs -1.4 pg/mL and -1.9 pg/mL, respectively, P = 0.52). The ghrelin/obestatin ratio for the initial and week 8 levels changed significantly in only the H. pylori eradicated group (0.11 vs 0.08, respectively, P = 0.015). For overweight patients (as designated by body mass index), we observed significant increases in obestatin levels in the eradicated group as compared to non-eradicated group (201 ± 458 pg/mL vs -5 ± 81 pg/mL, respectively, P = 0.02). In the H. pylori-eradicated group, the levels did not differ between the sexes for ghrelin (-6.3 ± 26.9 pg/mL vs -8.0 ± 24.0 pg/mL, respectively, P = 0.97) or obestatin (210 ± 390 pg/mL vs 96 ± 372 pg/mL, respectively, P = 0.23).
CONCLUSION: Serum levels of ghrelin decreased while obestatin levels increased in H. pylori eradicated subjects, especially in overweight and male patients.
PMCID: PMC3631992  PMID: 23613634
Ghrelin; Obestatin; Helicobacter pylori; Gastric peptides; Appetite
20.  Serological diagnosis of Helicobacter pylori--evaluation of four tests in the presence or absence of non-steroidal anti-inflammatory drugs. 
Gut  1993;34(4):461-465.
The host's humoral immune response to Helicobacter pylori has been used in the diagnosis of active infection with these organisms. Several commercial tests are available but there are few and unconfirmed reports of their efficacy. This study aimed to assess and compare the efficacy of the following H pylori serological tests in patients treated or not treated with non-steroidal anti-inflammatory drugs (NSAID): Pyloriset Latex, Helico-G, Biolab Malakit, and Bio-Rad GAP Test IgG. Venous blood was tested at random in 124 patients, 64 of whom had received NSAID and 60 who had not. H pylori IgG antibodies were detected by latex agglutination (Pyloriset), or by ELISA (the remaining tests). Endoscopic gastric antral biopsy specimens were also obtained for urease activity, culture, and histology. Detection of H pylori by at least two of these was considered as a true positive, and its absence in all biopsy specimens as a true negative. The sensitivity values in the presence (or absence) of NSAID were: Pyloriset Latex, 59 (60)%; Helico-G, 79 (74)%; Biolab Malakit, 85 (81)%; and Bio-Rad GAP Test IgG, 100 (95)%. The respective specificity values were: 50 (71)%, 47 (59)%, 50 (65)%, and 30 (29)%. The Bio-Rad GAP Test IgG has the highest sensitivity and the lowest specificity values regardless of NSAID intake. The sensitivity of the other tests, however, is less than that of the standard biopsy related tests and their specificity is even lower in chronic NSAID users.
PMCID: PMC1374303  PMID: 8491390
21.  Presence of Helicobacter pylori in betel chewers and non betel chewers with and without oral cancers 
BMC Oral Health  2009;9:23.
Betel chewing has been shown to predispose to periodontal disease and oral cancer. Studies show that people with gum disease are more likely to test positive for Helicobacter pylori (H. pylori). It is not known if the lesions produced by betel quid and the resulting, chemical changes predispose to colonization by H. pylori. Further the role of this organism in oral cancer is not known. Our objective was to determine the presence of H. pylori in oral lesions of thirty oral cancer patients and to determine the presence of IgG antibodies to H. pylori in oral cancer patients who are betel chewers and non betel chewers, healthy betel chewers and healthy non-betel chewers and to compare the presence of H. pylori in these four groups. This case control study was conducted at the Cancer Institute Maharagama and the Department of Microbiology, Faculty of Medical Sciences, University of Sri Jayewardenepura.
One hundred and seventy three subjects, of whom fifty three were patients presenting with oral cancer to the Cancer Institute Maharagama, sixty healthy betel chewers and sixty healthy non-betel chewers from the Religious and Welfare Service Centre Maharagama were tested for H. pylori by serology. Thirty oral biopsies from oral cancer patients were cultured under microaerophilic condition to isolate H. pylori. The statistic used was Chi-square test.
Of the fifty-three oral cancer patients, forty-four were betel chewers. Among the 53 oral cancer patients examined, ten of forty-four (10/44 = 22.7%) patients who are betel chewers and four of nine (4/9 = 44.4%) patients who are non-betel chewers were detected positive for IgG antibody against H. pylori. In the healthy group (betel chewers and non betel chewers) ten (16.7%) of the healthy betel chewers tested positive for H. pylori by serology. None of the healthy non-betel chewers tested positive for H. pylori
Fourteen [26.4%] of oral cancer patients tested positive for H. pylori by serology, of which two were also culture positive (Only thirty samples were cultured). The presence of H. pylori in betel chewers (with or without cancer) compared to non-betel chewers was statistically significant. (Chi-square test p < 0.05) The use of tobacco and areca nut in betel chewers was significant with the presence of H. pylori (p < 0.05).
There is a significant higher proportion of H. pylori in betel chewers compared to non-betel chewers but not between oral cancer patients compared to patients without oral cancer. Hence Betel chewing may predispose to colonisation with H. pylori in the digestive tract through swallowing the quid or during betel chewing.
PMCID: PMC2755467  PMID: 19772630
22.  Influence of Helicobacter pylori infection on ghrelin levels in children 
AIM: To compare ghrelin levels in plasma and gastric mucosa before and after Helicobacter pylori (H. pylori) treatment in children with H. pylori-associated functional dyspepsia.
METHODS: Children with H. pylori-associated functional dyspepsia were enrolled in this study. H. pylori infection was confirmed by positive bacterial culture results. All of the children received triple H. pylori eradication therapy (a 2 wk course of omeprazole, amoxicillin, and clarithromycin). The children were divided into two groups based on the success of the H. pylori treatment: group 1 (eradicated) - patients who had a negative 13C-urea breath test 2 mo after the end of therapy; and group 2 (non-eradicated) - patients who had a positive 13C-urea breath test. Plasma ghrelin, gastric ghrelin mRNA, and the body mass index were evaluated in both groups before and after the H. pylori treatment. The plasma ghrelin levels were measured by a radioimmunoassay. The expression of gastric ghrelin mRNA was determined by real-time reverse transcription polymerase chain reaction.
RESULTS: A total of 50 children with H. pylori-associated functional dyspepsia were treated with triple H. pylori eradication therapy. The mean age of the children was 5.52 ± 0.83 years, and there were 28 males and 22 females. Among the 50 H. pylori-positive children, 30 successfully achieved eradication, and 20 did not. The mean plasma ghrelin levels of group 1 were 22.17 ± 1.73 ng/L and 26.59 ± 2.05 ng/L before and after the treatment, respectively, which was a significant increase (P = 0.001). However, the mean plasma ghrelin level of group 2 before and after the H. pylori treatment was 21.34 ± 2.40 ng/L and 22.24 ± 2.10 ng/L (P = 0.785). The plasma ghrelin levels increased substantially after treatment in group 1 but showed only minor changes in group 2. Similarly, the gastric ghrelin mRNA expression in group 1 before treatment was 2.84 ± 0.08. After treatment, the level was 3.11 ± 0.65, which was significantly different (P = 0.023). The gastric ghrelin mRNA expression in group 2 did not change significantly during the treatment (2.82 ± 0.44 vs 2.79 ± 0.31, P = 0.875). The plasma ghrelin and gastric ghrelin mRNA levels in group 1 increased substantially after the treatment but did not do so in group 2. In addition, the body mass index the two groups did not differ significantly 2 mo before and after the H. pylori treatment.
CONCLUSION: H. pylori eradication increases the plasma and tissue ghrelin levels in children with H. pylori-associated functional dyspepsia.
PMCID: PMC3460338  PMID: 23049220
Helicobacter pylori; Functional dyspepsia; Ghrelin; Eradication; Children
23.  Rapid colorimetric hybridization assay for detecting amplified Helicobacter pylori DNA in gastric biopsy specimens. 
Journal of Clinical Microbiology  1996;34(3):530-533.
A very simple, practical, sensitive, and specific colorimetric hybridization assay for detecting amplified Helicobacter pylori DNA is described. This assay, which combines a sensitive sandwich DNA hybridization reaction and a colorimetric protocol similar to those used in conventional enzyme immunoassays, was shown to be suitable for detecting H. pylori-infected gastric biopsy specimens and for monitoring the eradication of the pathogen after treatment. The specificity and sensitivity of the colorimetric hybridization assay were tested by assaying 27 H. pylori strains (4 reference and 23 clinical isolates), 9 strains of other Helicobacter spp. or Campylobacter spp., and 11 clinical isolates of other urease-positive bacteria. The likelihood of H. pylori detection in gastric biopsy specimens by the colorimetric hybridization assay was evaluated with 23 H. pylori-positive and 41 H. pylori-negative biopsy specimens on the basis of positive and negative results, respectively, of culture, rapid urease test, histological examination, and PCR. Biopsy specimens from 33 treated patients, endoscopied 4 to 8 weeks after the end of treatment, were also tested. All H. pylori strains showed positive results in the colorimetric hybridization assay, presenting optical densities at 450 nm (OD450S) of > or = 3.0. None of the other Helicobacter spp., Campylobacter spp., or the clinical isolates of other urease-positive bacteria showed OD450S equal to or greater than the cutoff (mean OD450 cutoff, 0.208). The colorimetric hybridization assay detected all 23 H. pylori-positive biopsy specimens (mean OD450, 2.910 +/- 0.295), while none of the H. pylori-negative biopsy specimens was shown to be positive in the assay (mean OD450, 0.108 +/- 0.025). H. pylori was considered to be not eradicated from three of the posttreatment biopsy specimens by culture, rapid urease test, histological examination, and PCR. They were all positive by the colorimetric hybridization assay, and their OD450S were > or = 3.0. The colorimetric hybridization assay also detected two other H. pylori-positive patients. Specimens from these two patients had negative culture, rapid urease test, and histology results, and a specimen from one of them also tested negative by PCR. These results indicate that the colorimetric hybridization assay is a suitable method both for the diagnosis of H. pylori in biopsy specimens and for the follow-up of patients after the end of treatment.
PMCID: PMC228840  PMID: 8904408
24.  Acute perforated duodenal ulcer is not associated with Helicobacter pylori infection. 
Gut  1993;34(10):1344-1347.
Most patients with chronic duodenal ulcer disease have Helicobacter pylori infection and eradicating it considerably reduces the relapse rate. The prevalence of H pylori in 80 patients (mean age = 52 years, range 17-85) presenting with acute perforated duodenal ulcer was examined and compared with age and sex matched hospital control patients. H pylori state was assessed by serum anti-H pylori IgG (Helico-G kit, Porton) using a titre of 18 or less as negative with a specificity of 89% and sensitivity of 88%. Only 47% of the perforated duodenal ulcer patients were positive for H pylori and this was similar to the value of 50% in the controls. In 51 of the perforated duodenal ulcer patients 14C-urea breath tests were also performed 4-10 weeks after surgery and this confirmed that only 49% were positive for H pylori. None of these patients had received perioperative drugs that might have eradicated the infection. The H pylori positive and H pylori negative perforated duodenal ulcer patients were similar with respect to age (53, 51), smoking (84%, 83%), and consumption of more than 15 units of alcohol per week (42%, 38%). Duodenal ulcer disease had been diagnosed before acute perforation in only 24% of those with H pylori and also 24% of those without the infection. Regular non-steroidal anti-inflammatory drug (NSAID) use was common in both those with (44%) and without (45%) H pylori. In conclusion, the lack of association of acute perforated duodenal ulcer and H pylori infection suggests that perforated duodenal ulcer has a different pathogenesis from chronic duodenal ulcer disease, and that the first should not be regarded simply as a complication of the second.
PMCID: PMC1374538  PMID: 8244099
25.  Evaluation of a Commercial Immunoblot, Helicoblot 2.1, for Diagnosis of Helicobacter pylori Infection ▿  
Clinical and Vaccine Immunology : CVI  2008;15(11):1705-1710.
The best method to diagnose Helicobacter pylori infection in different clinical situations is controversial. The aim of the study was to assess the performance of a commercial immunoblot, Helicoblot 2.1. The study comprised 215 patients, who were grouped according to the presence of H. pylori infection (assessed by two gastroscopies including histology with a median interval of 7.1 years, enzyme immunoassay [EIA]-based serology, and history of previous H. pylori infections and eradication therapies) into four categories: no H. pylori infection ever, previous infection, ongoing infection, and EIA seropositivity as the only marker of a possible previous infection. The sensitivity of Helicoblot 2.1 to show an ongoing or previous H. pylori infection was 100% and 92%, respectively. Helicoblot 2.1 was negative in only 80% of individuals with no evidence of present or previous infection but in 96% of patients 50 years of age or younger. The current infection marker of the immunoblot was positive in 49% of patients with successful H. pylori eradication therapy. After successful eradication therapy, Helicoblot 2.1 sustained positive results in 87% of patients, and CagA positivity was detected in 87% of patients with follow-up samples for more than 10 years after therapy. Helicoblot 2.1 is a sensitive and, among patients of ages 50 years or younger, a specific test in the primary diagnosis of H. pylori infection. However, it does not discriminate between past and current infections. It can be used in epidemiological studies assessing the role of H. pylori in different late sequelae.
PMCID: PMC2583517  PMID: 18827192

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