Overall and Stratified Accuracies of H. pylori Serology Testing: A Multicenter Study of 8497 Screening-Naïve Adults.

Diagnostic methods for H. pylori infection: Choices, opportunities and pitfalls.

Atrophic gastritis is a precancerous condition that is commonly caused by chronic Helicobacter pylori (H. pylori) infection. This blinded, controlled study was designed to determine if serum gastrin and pepsinogens were reliable markers of atrophy in asymptomatic patients. One hundred and forty-seven asymptomatic patients underwent endoscopy with multiple gastric biopsies obtained for histology, culture, and rapid urease test. Fasting serum gastrin (total and G-17) and serum pepsinogens (I-II) were determined by standard immunoassays. Gastric atrophy was histologically assessed in accordance with internationally accepted criteria; three main patterns of gastritis were distinguished: (a) nonatrophic gastritis, (b) atrophic antrum-restricted and antrum-predominant gastritis, and (c) corpus-restricted gastritis. Receiving operating characteristic (ROC) analysis was used to determine the best cut-off for each serum test in nonatrophic gastritis versus antrum-restricted/antrum-predominant atrophic gastritis. No significant differences in serum gastrin and pepsinogens I-II were detected in nonatrophic gastritis versus patients with antrum-restricted/antrum-predominant atrophic gastritis. The positive likelihood ratios for an abnormal serum test to detect antrum-restricted/antrum-predominant atrophy in the gastric body were total serum gastrin 2.13 (95% CI 0.99, 4.6), gastrin-17: 1.55 (95% CI 0.75, 36.17), pepsinogen I: 2.74 (1.4, 5.4), pepsinogen II: 1.74 (1.27, 2.39), and the ratio of pepsinogen I and II: 1.8 (1.2-2.8). Negative likelihood ratios ranged from 0.20 to 0.65. In an asymptomatic population, serum gastrin (total and G-17) and pepsinogens I-II (and their ratio) do not discriminate nonatrophic versus antrum-restricted/predominant atrophic gastritis.

3][4] In regions with low H. pylori prevalence, a test-and-treat strategy is usually recommend for those with dyspeptic symptoms but without so-called "alarm symptoms" such as weight loss, dysphagia, nausea, and vomiting.In that situation, noninvasive testing using the urea breath test (UBT), which shows high sensitivity (88% to 95%) and specificity (95% to 100%), is recommended along with a stool antigen test that shows similar diagnostic accuracy. 2However, the "endoscope-and-treat" approach is recommended in regions with high prevalence of H. pylori and high incidence of gastric cancer such as in South Korea.When endoscopy is performed, a biopsy-based test, such as the rapid urease test (RUT), histological evaluation, and H. pylori culture can be performed to confirm the current infection.The RUT is the most sensitive and specific of these tests (sensitivity, 85% to 97%; specificity, 92%). 4he RUT is based on detecting activity of the urease enzyme, which breaks down urea to ammonia, increasing the pH of the medium.The CLOtest TM (Delta West Ltd., Bentley, Australia) is the most frequently used commercially available RUT kit and provides results within 24 hours.Previous studies have evaluated the optimal site and number of gastric muco-

BackgroundHuman pepsinogens are considered promising serological biomarkers for the screening of atrophic gastritis (AG) and gastric cancer (GC). However, there has been controversy in the literature with respect to the validity of serum pepsinogen (SPG) for the detection of GC and AG. Consequently, we conducted a systematic review and meta-analysis to assess the diagnostic accuracy of SPG in GC and AG detection.MethodsWe searched PubMed, Embase, and the Chinese National Knowledge Infrastructure (CNKI) for correlative original studies published up to September 30, 2014. The summary sensitivity, specificity, positive diagnostic likelihood ratio (DLR+), negative diagnostic likelihood ratio (DLR-), area under the summary receiver operating characteristic curve (AUC) and diagnostic odds ratio (DOR) were used to evaluate SPG in GC and AG screening based on bivariate random effects models. The inter-study heterogeneity was evaluated by the I2 statistics and publication bias was assessed using Begg and Mazumdar’s test. Meta-regression and subgroup analyses were performed to explore study heterogeneity.ResultsIn total, 31 studies involving 1,520 GC patients and 2,265 AG patients were included in the meta-analysis. The summary sensitivity, specificity, DLR+, DLR-, AUC and DOR for GC screening using SPG were 0.69 (95% CI: 0.60–0.76), 0.73 (95% CI: 0.62–0.82), 2.57 (95% CI: 1.82–3.62), and 0.43 (95% CI: 0.34–0.54), 0.76 (95% CI: 0.72–0.80) and 6.01 (95% CI: 3.69–9.79), respectively. For AG screening, the summary sensitivity, specificity, DLR+, DLR-, AUC and DOR were 0.69 (95% CI: 0.55–0.80), 0.88 (95% CI: 0.77–0.94), 5.80 (95% CI: 3.06–10.99), and 0.35 (95% CI: 0.24–0.51), 0.85 (95% CI: 0.82–0.88) and 16.50 (95% CI: 8.18–33.28), respectively. In subgroup analysis, the use of combination of concentration of PGI and the ratio of PGI:PGII as measurement of SPG for GC screening yielded sensitivity of 0.70 (95% CI: 0.66–0.75), specificity of 0.79 (95% CI: 0.79–0.80), DOR of 6.92 (95% CI: 4.36–11.00), and AUC of 0.78 (95% CI: 0.72–0.81), while the use of concentration of PGI yielded sensitivity of 0.55 (95% CI: 0.51–0.60), specificity of 0.79 (95% CI: 0.76–0.82), DOR of 6.88 (95% CI: 2.30–20.60), and AUC of 0.77 (95% CI: 0.73–0.92). For AG screening, the use of ratio of PGI:PGII as measurement of SPG yielded sensitivity of 0.69 (95% CI: 0.52–0.83), specificity of 0.84 (95% CI: 0.68–0.93), DOR of 11.51 (95% CI: 6.14–21.56), and AUC of 0.83 (95% CI: 0.80–0.86), the use of combination of concentration of PGI and the ratio of PGI:PGII yield sensitivity of 0.79 (95% CI: 0.72–0.85), specificity of 0.89 (95% CI: 0.85–0.93), DOR of 24.64 (95% CI: 6.95–87.37), and AUC of 0.87 (95% CI: 0.81–0.92), concurrently, the use of concentration of PGI yield sensitivity of 0.46 (95% CI: 0.38–0.54), specificity of 0.93 (95% CI: 0.91–0.95), DOR of 19.86 (95% CI: 0.86–456.91), and AUC of 0.86 (95% CI: 0.52–1.00).ConclusionSPG has great potential as a noninvasive, population-based screening tool in GC and AG screening. In addition, given the potential publication bias and high heterogeneity of the included studies, further high quality studies are required in the future.

Helicobacter pylori infection has been considered to play significant role in gastric carcinogenesis, but only a minority of people who harbor this organism will develop gastric cancer. H. pylori infection first causes chronic non atrophic gastritis. Chronic non atrophic gastritis may evolve to atrophic gastritis and intestinal metaplasia and finally to dysplasia and adenocarcinoma. To estimate the prevalence of H. pylori infection and the precancerous gastric lesions and their relationship, in patients with dyspeptic symptoms who underwent upper gastrointestinal endoscopy at a reference center in the central region of Rio Grande do Sul state, Brazil. We analyzed gastric biopsies taken from corpus and antrum of patients who underwent upper gastrointestinal endoscopy for H. pylori detection, between 1994 and 2003. According to Sydney system, chronic non atrophic gastritis, atrophic gastritis and intestinal metaplasia were diagnosed by histological examination (H-E stain). The histological diagnoses were related to H. pylori infection status. Biopsies from 2,019 patients were included in the study. Patients mean age was 52 (+/-15) and 59% were female. Seventy six percent had H. pylori infection. Normal mucosa, chronic non atrophic gastritis, atrophic gastritis and intestinal metaplasia were diagnosed in 5%, 77%, 3% and 15%, respectively. The OR for any degree of gastric mucosa lesion in infected patients was 10 (CI95% 6.50 - 17%). The OR for infected patients had chronic non atrophic gastritis was 3 (CI95% 2,2 - 3,4). The OR for infected patients had atrophic gastritis or intestinal metaplasia was less than 1. The prevalence of H. pylori infection in this population was high (76%) and infected individuals had the probability 10 folds greater than non infected individuals to have any lesion of gastric mucosa. The prevalence of precancerous lesions was 77% for non atrophic chronic gastritis, 3% for atrophic gastritis and 15% for intestinal metaplasia. Infected patients had risk 3 folds greater than non-infected for the occurrence of non atrophic chronic gastritis. H. pylori infection did not show risk for occurrence of atrophic gastritis and intestinal metaplasia, suggesting that other risk factors should be involved in the carcinogenesis process.

Helicobacter pylori infection inhibits reflux esophagitis by inducing atrophic gastritis

Currently the screening and diagnosis of gastric cancer and atrophic gastritis are mainly made by endoscopy and biopsy. The aim of this study was to evaluate the use of serum tests: serum pepsinogen I (PGI pepsinogen I/II ratio (PGR), gastrin-17 (G-17) and H. pylori-immunoglobulin G (IgG) antibodies to screen atrophic gastritis and gastric cancer. A total of 458 patients were recruited, and each underwent endoscopy with biopsies before the serum tests were performed. These patients were divided into five groups based on the endoscopic and histological findings: 92 patients in the atrophic gastritis group, 58 in the gastric ulcer group, 90 in the duodenal ulcer group, 141 in the gastric cancer group (40 early gastric cancer and 101 advanced gastric cancer) and 77 (including mild non-atrophic gastritis) served as a control group. Serum samples for PGI and II, G-17, and H. pylori-IgG antibodies estimation were analyzed by ELISA. PGI and PGR values decreased significantly both in atrophic gastritis and gastric cancer groups (P<0.01). For the best discrimination of atrophic gastritis, the cut-off values of PGI and PGR were 82.3 microg/L and 6.05, respectively. The PGI, PGR and G-17 values were related significantly with the grades and/or sites of atrophic gastritis (P<0.01). Patients with atrophic corpus gastritis had low PGI and PGR values and high G-17 level, and patients with atrophic antral gastritis had low G-17 level. G-17 increased significantly in the gastric cancer group (P<0.01). PGI and PGR values were significantly lower in patients with advanced gastric cancer than in patients with early gastric cancer, while there was no difference in G-17 level between them. The positivity rate of H. pylori-IgG antibodies was 54.55% in the control group. The PGI level was higher in H. pylori positive patients than in H. pylori negative ones (P<0.001), while there was no difference in G-17 level between them. The positivity rates of H. pylori-IgG antibodies were over 85% in all other four groups. Low serum PGI, PGR and G-17 values are biomarkers of atrophic antral gastritis. Atrophic be screened by serum PGI and PGR values. Gastric cancer can be screened on the basis of increased serum G-17 and remarkedly low serum PGI and PGR values. The H. pylori infection is related to the change of PG level.

Objective: This study aimed to evaluate the optimal biopsy site for Helicobacter pylori detection by comparing the results of rapid urease test (RUT) between the gastric corpus and the antrum.Methods: A biopsy specimen from each subject was obtained from the corpus and from the antrum. For each subject, the two specimens were separately immersed in two different RUT kits. Positive reaction times were measured at 20 minutes and 1, 3, and 24 hours. If either of the two RUT kits showed a positive reaction, H. pylori infection was confirmed.Results: A total of 310 H. pylori-infected subjects were eligible for study inclusion. Compared with the antrum, positive RUT reaction times in the corpus were shorter when the degree of gastric atrophy was moderate or severe (p = .001 and p < .001, respectively). A multivariate analysis revealed that the factors resulting in a faster positive RUT reaction in the corpus were age ≥50 years (odds ratio [OR] = 1.84; 95% confidence interval [CI] = 1.10–3.08; p = .021) and severe gastric atrophy (OR = 2.41; 95% CI = 1.13–5.13; p = .023). Also, severe gastric atrophy was an independent factor associated with positive RUT reaction only in the corpus (OR = 5.12; 95% CI = 1.55–16.88; p = .007).Conclusions: In subjects aged ≥50 years or with severe gastric atrophy, biopsy of the corpus mucosa optimized the efficiency of H. pylori detection through a faster positive RUT reaction.

Although it is widely accepted that Helicobacter pylori (H. pylori) infection is an important cause of atrophic gastritis, few studies have examined the relationship between H. pylori-induced atrophic gastritis and the occurrence of reflux esophagitis. The present study was aimed to examine the relationship between H. pylori infection, atrophic gastritis, and reflux esophagitis in Japan. A total of 175 patients with reflux esophagitis were compared with sex- and age-matched 175 control subjects. Diagnosis of H. pylori infection was made by gastric mucosal biopsy, rapid urease test, and serum IgG antibodies. Severity of atrophic gastritis was assessed by histology and serum pepsinogen I/II ratio. H. pylori infection was found in 59 (33.7%) patients with reflux esophagitis, whereas it was found in 126 (72.0%) control subjects. The grade of atrophic gastritis was significantly lower in the former than in the latter. Among the H. pylori-positive patients, atrophic gastritis was milder in the patients with reflux esophagitis than in the patients without it. These findings suggest that most cases of reflux esophagitis in Japan occur in the absence of H. pylori infection and atrophic gastritis, and it may also tend to occur in patients with milder gastritis even in the presence of H. pylori infection. Therefore, H. pylori infection may be an inhibitory factor of reflux esophagitis through inducing atrophic gastritis and concomitant hypoacidity.

Detection of Helicobacter pylori in adenotonsillar tissue of children with chronic adenotonsillitis using rapid urease test, PCR and blood serology: A prospective study

Helicobacter pylori colonization on tonsil tissue

Introduction: Patients with Chronic Atrophic Gastritis (CAG) and Gastric Intestinal Metaplasia (GIM) are at risk of developing gastric adenocarcinoma. The early and accurate detection of these lesions is critical for effective intervention and improved patient outcomes. Aim: To study the Sydney protocol and targeted single-site biopsy in detecting premalignant gastric lesions, identifying the most reliable method for early diagnosis. Materials and Methods: This was a cross-sectional study conducted in the Department of Pathology and Laboratory Medicine at Jagjivan Ram Hospital, Western Railway, Mumbai, Maharashtra, India from June 2023 to February 2024. A total of 100 gastric biopsies were included, comprising 50 cases of targeted single-site biopsy and 50 cases following the Sydney protocol. The Sydney protocol recommends obtaining biopsies from five specific sites in the stomach: two from the antrum, two from the body and one from the incisura angularis. The parameters studied were atrophy and intestinal metaplasia, which were assessed using histopathological evaluation of gastric biopsy specimens. The results were analysed by calculating interobserver agreement using kappa statistics to evaluate the reproducibility and reliability of the diagnostic criteria. Results: Out of 50 targeted single-site biopsies, urease was positive in 14 (28%) cases. A total of 14 (28%) patients had CAG, of which 12 were stage I and 2 were stage II. A total of 4 (8%) patients had intestinal metaplasia, out of which three were stage I and one was stage II. Out of 50 Sydney protocol-compliant biopsies, 20 (40%) patients’ urease tests were positive in at least one biopsy site. A total of 30 (60%) patients had CAG, of which 15 (30%) had CAG in all three sites (corpus, antrum and incisura), 4 (8%) had CAG only in the corpus, 4 (8%) had CAG only in the antrum, 3 (6%) had CAG in both the antrum and incisura, 2 (4%) had CAG in both the corpus and incisura, and 2 (4%) had CAG only in the corpus. Out of these 30 patients with CAG, 18 (36%) were classified as stage I, 9 (18%) as stage II, and 3 (6%) as stage III. A total of 10 (20%) patients had GIM, of which 6 (12%) had GIM only in the antrum, 2 (4%) had intestinal metaplasia in both the corpus and antrum, 1 (2%) had intestinal metaplasia in both the antrum and incisura and 1 (2%) had intestinal metaplasia only in the incisura. Out of these 10 patients with intestinal metaplasia, 5 (10%) were classified as stage I, 3 (6%) as stage II, 1 (2%) as stage III, and 1 (2%) as stage IV. Additionally, 3 (6%) patients had low-grade dysplasia. Conclusion: The Sydney protocol outperforms targeted singlesite biopsy in detecting premalignant gastric lesions due to its comprehensive sampling from multiple sites, thereby reducing the risk of missed lesions. This thorough approach ensures accurate diagnosis and highlights the importance of endoscopic follow-up for ongoing patient management.

BackgroundIt has been suggested that GastroPanel might be a useful tool for the diagnosis of chronic atrophic gastritis (CAG) measuring four biomarkers in blood: basal gastrin-17 (G17), pepsinogen I and II (PGI and PGII), and Helicobacter pylori antibodies.AimTo determine the accuracy of GastroPanel for the diagnosis of CAG.MethodsThis was a prospective, blinded, multicenter study that included dyspeptic patients. G17, PGI, and PGII were determined by enzyme immunoassays. Three antrum and two corpus biopsies were obtained for standard histological analysis and rapid urease test. Biopsies were analyzed by a single blinded expert pathologist.ResultsNinety-one patients were included (77% women, mean age 44 years, 51% H. pylori positive, 17% with CAG). G17 was reduced in patients with antrum CAG (5.4 vs. 13.4 pmol/l; P<0.01) and increased in patients with corpus CAG (11 vs. 24 pmol/l; P<0.05), but its accuracy was only acceptable in the case of corpus localization [area under the receiver operating characteristic curve (AUC), 74%]; PGII difference was almost statistically significant only when testing for corpus atrophy (33 vs. 21 μg/l; P=0.05; AUC=72%). The PGI and PGI/PGII ratio showed no significant differences (AUCs were all unacceptably low). Helicobacter pylori antibody levels were higher in H. pylori-infected patients (251 vs. 109 EIU, P=0.01; AUC=70). The accuracy of GastroPanel for the diagnosis of CAG was as follows: sensitivity 50%; specificity 80%; positive 25% and negative 92% predictive values; and positive 2.4 and negative 0.6 likelihood ratios.ConclusionGastroPanel is not accurate enough for the diagnosis of CAG; thus, its systematic use in clinical practice cannot be recommended.

Background/objective: H. pylori infection is commonly diagnosed using an anti-H. pylori IgG antibody test. However, a proportion of results are falsely sero-negative. We investigated characteristics of patients falsely seronegative for H. pylori in relation to gastric atrophy. Methods: H. pylori infection (Hp+ or Hp-) was determined based on culture test, rapid urease test (RUT), and polymerase chain reaction (PCR) test in 280 outpatients. Anti-H. pylori antibody titers ≥ 10 U/ml were diagnosed as sero-positive for H. pylori (IgG+), while those <10 U/ml were sero-negative (IgG-). Serum pepsinogen (PG) I/PG II ratios were calculated as a serological marker of gastric atrophy. Endoscopic gastric mucosal atrophy was also assessed according to the Kimura-Takemoto classification system. Results: The mean PG I/PG II ratio in each group was as follows: Hp-/IgG- (4.99 ± 1.04, n=10), Hp+/IgG+ (2.59 ± 1.51, n=240), Hp-/IgG+ (5.65 ± 2.72, n=4) and Hp+/IgG- (3.02 ± 2.61, n=26). The mean serum PG I/PG II ratio in the Hp+/IgG- group was lower than those of Hp-/IgG- and Hp-/IgG+ groups (P=0.028 and 0.072). Incidence of severe gastric mucosal atrophy in the Hp+/IgG- group was highest of the four groups. Conclusions: Individuals falsely sero-negative for H. pylori infection is at increased risk of severe atrophic gastritis, which is well known as precancerous lesion.

Background: Ghrelin, an orexigenic hormone, has multiple favorable functions including protein anabolism enhancement, anti-inflammatory actions, and cardiovascular protection. A low plasma ghrelin level is associated with increased mortality in patients treated with hemodialysis (HD). However, it is unclear whether the plasma ghrelin level in HD patients correlates with the severity of gastric mucosal atrophy and Helicobacter pylori status. Methods: Seventy-eight maintenance HD patients and 51 non-dialysis patients with chronic kidney disease were evaluated for severity of gastric mucosal atrophy by gastroduodenoscopy and for H. pylori status using an anti-H. pylori-antibody and rapid urease test. Plasma acyl and des-acyl ghrelin levels were measured and their associations with relevant clinical parameters were investigated. Results: Des-acyl ghrelin level in HD patients was significantly higher than that in patients with kidney function preserved. Although acyl and des-acyl ghrelin levels were similar between current H. pylori positive and negative HD patients, both levels decreased significantly with the progress of endoscopic gastric mucosal atrophy in HD patients. Serum pepsinogen (PG) I level and PG I/II ratio decreased significantly according to the severity of atrophy in HD patients and positively significantly correlated with both ghrelin levels. Multiple regression analysis showed significant positive correlations between acyl ghrelin and PG I levels (β = 0.738, p < 0.001) and significant negative correlations between ghrelin and age, albumin, and creatinine levels. Conclusions: Gastric atrophy is the major determinant of ghrelin level in HD patients. Management practices, such as H. pylori eradication, before advanced atrophy may be required to prevent the decrease of ghrelin levels and improve the prognosis of HD patients.