Serum pepsinogen (PG) is a good indicator of atrophic changes in the gastric mucosa. Gastric mucosal atrophy is a high-risk factor for gastric cancer. Serological testing for PG combined with endoscopy can help to improve gastric cancer screening. In this study, we established the reference ranges of serum PG-I, PG-II, and the PG-I/II ratio (PGR) in the Chinese population by chemiluminescence immunoassay (CLIA) and enzyme-linked immunosorbent assay (ELISA). Besides, in the real world, doctors are often confused by the results of different testing platforms. Thus, a comparison of methods CLIA and ELISA was performed.

2904 individuals were enrolled from six regions in China as part of the Chinese Adult Digestive Diseases Surveillance (2016) program. The individuals completed questionnaires and volunteered to undergo examinations, including gastroscopy, urea breath test, abdominal ultrasound examination and routine serologic tests. Serum was collected to measure PGs (including PG-I, PG-II and PGR) by CLIA and ELISA. Participants who were found obvious abnormalities or absent from the examinations were excluded. Ultimately, 747 healthy individuals were enrolled in this study. The Kolmogorov-Smirnov test was used to assess the distribution of variables. The Kruskal-Wallis H or Mann-Whitney U-tests were used to compare different sex, age, and geographical groups. The 95% reference ranges of PGs obtained by the two methods were established according to document CLSI-EP28-A3, with covariates of sex, age, and region. Spearman correlation analysis, linear regression analysis and allowable total error (ATE) zone analysis were utilized for comparing the two methods.

On overall, the 95% reference ranges of PG-I, PG-II, and PGR measured by CLIA were 23.00-110.64 ng/mL, 2.50-19.13 ng/mL, and 3.87-13.30, respectively. Meanwhile, the reference ranges of PG-I, PG-II, and PGR measured by ELISA were 36.93-205.06 ng/mL, 1.65-17.96 ng/mL, and 7.50-33.60, respectively. Both PG-I and PG-II levels measured by the two platforms were found to be influenced by sex and age. PGR measured by CLIA was influenced by age but not by sex, while PGR measured by ELISA was not affected by either age or sex. Regional factors did not significantly impact the PG results, except for PG-I detected by ELISA. Ultimately, reference ranges for PGs were established based on age and sex stratification. Additionally, the Spearman correlation analysis revealed that the correlation coefficients for PG-I, PG-II, and PGR detected by the two methods were 0.899, 0.887, and 0.777, respectively, indicating a strong correlation between the two methods. The regression equation for the PG levels detected by two methods was obtained through linear regression analysis. The ATE analysis provided a visual depiction of the consistency between the two methods, clearly indicating the poor agreement between them.

This study established the reference ranges of PGs by strict and intact enrollment standard. In addition, the results indicated a strong linear relationship between the two methods, yet with a clear bias, which was valuable for laboratory interpretation.

Helicobacter pylori (H. pylori) infection is the most prevalent type of bacterial infection. Current guidelines from different regions of the world neglect specific African conditions and requirements. The African Helicobacter and Microbiota Study Group (AHMSG), founded in 2022, aimed to create an Africa-specific consensus report reflecting Africa-specific issues.

Eighteen experts from nine African countries and two European delegates supported by nine African collaborators from eight other countries prepared statements on the most important African issues in four working groups: (1) epidemiology, (2) diagnosis, (3) indications and prevention, and (4) treatment. Limited resources, restricted access to medical systems, and underdeveloped diagnostic facilities differ from those of other regions. The results of the individual working groups were presented for the final consensus voting, which included all board members.

There is a need for further studies on H. pylori prevalence in Africa, with diagnosis hinged on specific African situation. Treatment of H. pylori in the African setting should be based on accessibility and reimbursement, while indication and prevention should be defined in specific African countries.

Helicobacter pylori (H. pylori) infection is a high-risk factor for gastric cancer (GC). The main aim of this study was to evaluate the effect of H. pylori on gastritis staging systems and the value of H. pylori combined with gastritis staging systems in predicting GC risk.

This study enrolled 609 patients with gastric atrophy (GA) and 527 patients with gastric intestinal metaplasia (GIM), who were graded by the OLGA and OLGIM staging systems, respectively. Each individual underwent serum pepsinogen (PG) test, H. pylori detection and questionnaire investigation. We did a real-world retrospective follow-up survey for them in April 2022.

Compared with H. pylori-negative patients, H. pylori-positive patients had higher serum PGs/gastrin-17 (G-17) levels and lower PGR levels, regardless of OLGA/OLGIM stages I-II or III-IV. Furthermore, eight patients with atrophic gastritis who progressed to GC were previously in OLGA stages III-IV and OLGIM stages II-IV. The average duration of this process was 2.19±1.03 years. Logistic regression analysis indicated that PGI and H. pylori infection were independent risk factors of individuals with OLGA stages III-IV. Age and PGR were independent risk factors of patients with OLGIM stages III-IV. PGI and PGR had good clinical diagnostic values for OLGA stages III-IV and OLGIM stages III-IV, respectively.

Patients with OLGA/OLGIM stages III-IV should undergo endoscopic surveillance regardless of H. pylori infection. H. pylori-positive patients with OLGIM stage II also have a high risk of GC. H. pylori combined with PGI and PGR is helpful to evaluate the severity of chronic gastritis.

Purpose: It is very essential to diagnose gastric atrophy in the area with high prevalence of gastric cancer. Operative link for gastritis assessment (OLGA) was developed to detect the severity of gastric atrophy. The aim of this study was to develop and validate nomograms for predicting OLGA any-stage and stages III-IV in the Chinese high-risk gastric cancer population. Methods: We retrospectively analyzed 7,945 participants obtained by a multicenter cross-sectional study. We randomly selected 55% individuals (4,370 participants, training cohort) to analyze and generate the prediction models and validated the models on the remaining individuals (3,575 participants, validation cohort). A multivariate logistic regression model was used to select variables in the training cohort. The corresponding nomograms were developed to predict OLGA any-stage and stages III-IV, respectively. The area under the receiver operating characteristic curves and the GiViTI calibration belts were used to estimate the discrimination and calibration of the prediction models. Results: There were 1,226 (28.05%) participants in the training sample and 970 (27.13%) in the validation sample who were diagnosed with gastric atrophy. The nomogram predicting OLGA any-stage had an area under the curve (AUC) of 0.610 for the training sample and 0.615 for the validation sample, with favorable calibrations in the overall population. Similarly, the nomogram predicting OLGA stages III-IV had an AUC of 0.702 and 0.714 for the training and validation samples, respectively, with favorable calibrations in the overall population. Conclusions: The prediction model can early identify the occurrence of gastric atrophy and the severity stage of gastric atrophy to some extent.

Gastric cancer (GC) is the eighth most common cause of cancer deaths in Croatia and one of the most common causes of cancer deaths worldwide. A reliable diagnostic tool for the early detection of GC is essential.

We previously suggested a pepsinogen test method to reduce the mortality from GC by allowing early detection. Here, we report an updated analysis from a prospective single-center clinical study to evaluate the sensitivity and specificity of the pepsinogen test method and to determine whether this test can be used as a part of routine laboratory assessment of high-risk patients.

We present mature data of the pepsinogen test method in the Croatian population after a median follow-up of 36 months. Statistical analyses were performed using a Mann-Whitney U test, multiple logistic regression, and receiver operating characteristics (ROC) to evaluate the predictive power of the assayed biomarkers.

Of the 116 patients, 25 patients had GC and 91 demonstrated a nonmalignant pathology based on tissue biopsy. Cutoff values were pepsinogen I ⩽70 and pepsinogen I/II ratio ⩽3.0. Using ROC curve analysis, the accuracy, sensitivity, specificity, positive predictive value, and negative predictive value were determined to be 87.22%, 78.12%, 90.10%, 71.43%, and 92.86%, respectively, for the diagnosis of GC. The area under the curve was 0.700 (95% confidence interval 0.57-0.83).

Pepsinogen tests are valuable for screening a population in need of further diagnosis and could help to avoid unnecessary invasive endoscopic procedures.

We assessed the validity of using serum pepsinogen tests (sPGTs) to differentiate autoimmune atrophic gastritis (AAG) from environmental atrophic gastritis (EAG). We also investigated the correlation and prognostic value between disease stage, according to Operative Link for Gastritis Assessment (OLGA)/Operative Link on Gastric Intestinal Metaplasia Assessment (OLGIM), and sPGT results in patients with gastric atrophy.

We enroled 115 patients in this prospective study: 95 with atrophic gastritis (16 with AAG and 79 with EAG) and 20 non-atrophic gastritis. These patients, along with 32 control patients, underwent esophagogastroduodenoscopy. Atrophy and intestinal metaplasia of the gastric biopsy specimens were staged according to the OLGA/OLGIM staging systems.

The median (IQR) age of the patients (83 females (56.5%)) was 58 (46-67) years. Patients in the AAG group represented histologically advanced stages. The AAG group had lower pepsinogen (PG) I and II levels, as well as a lower PGI/PGII ratio, compared with the EAG group (p<0.01, p<0.05 and p<0.01, respectively). The optimal PGI/PGII ratio for predicting AAG was ≤1.9 (100% sensitivity and 100% specificity), and that for predicting EAG was ≤9.2 (47.5% sensitivity and 90.6% specificity). The OLGA/OLGIM stage was negatively correlated with the PGI level and PGI/PGII ratio. In the AAG group, four of five patients with low-grade dysplasia had OLGA/OLGIM stage III-IV disease.

sPGT may provide valuable information for differentiating advanced-stage AAG from EAG, and in patients with atrophic gastritis, use of sPGTs and OLGA/OLGIM staging together may predict gastric cancer risk.

Gastric adenocarcinoma carries a poor prognosis, in part due to the late stage of diagnosis. Risk factors include Helicobacter pylori infection, family history of gastric cancer-in particular, hereditary diffuse gastric cancer and pernicious anaemia. The stages in the progression to cancer include chronic gastritis, gastric atrophy (GA), gastric intestinal metaplasia (GIM) and dysplasia. The key to early detection of cancer and improved survival is to non-invasively identify those at risk before endoscopy. However, although biomarkers may help in the detection of patients with chronic atrophic gastritis, there is insufficient evidence to support their use for population screening. High-quality endoscopy with full mucosal visualisation is an important part of improving early detection. Image-enhanced endoscopy combined with biopsy sampling for histopathology is the best approach to detect and accurately risk-stratify GA and GIM. Biopsies following the Sydney protocol from the antrum, incisura, lesser and greater curvature allow both diagnostic confirmation and risk stratification for progression to cancer. Ideally biopsies should be directed to areas of GA or GIM visualised by high-quality endoscopy. There is insufficient evidence to support screening in a low-risk population (undergoing routine diagnostic oesophagogastroduodenoscopy) such as the UK, but endoscopic surveillance every 3 years should be offered to patients with extensive GA or GIM. Endoscopic mucosal resection or endoscopic submucosal dissection of visible gastric dysplasia and early cancer has been shown to be efficacious with a high success rate and low rate of recurrence, providing that specific quality criteria are met.

Mongolia has the highest mortality rate of gastric cancer. The early detection of cancer and down-staging screening for high risk patients are essential. Therefore, we aimed to validate serum markers for stratifying patients for further management.

Endoscopy and histological examination were performed to determine high risk and gastric cancer patients. Rapid urease test, culture and histological tests were performed to diagnose Helicobacter pylori infection. Serum pepsinogen (PG) I and II and anti-H. pylori IgG were measured by ELISA. Receiver Operating Characteristic analysis was used to extract the best cut-off point.

Totally 752 non-cancer and 50 consecutive gastric cancer patients were involved. The corpus chronic gastritis (72%: 36/50 vs. 56.4%: 427/752), corpus atrophy (42.0%: 21/50 vs. 18.2%: 137/752) and intestinal metaplasia (IM) (64.0%: 32/50 vs. 21.5%: 162/752) were significantly higher in gastric cancer than non-cancer patients, respectively. Therefore, corpus chronic gastritis, corpus atrophy and IM were considered as high risk disease. The best serum marker to predict the high risk status was PGI/II < 3.1 (sensitivity 67.2%, specificity 61%) and PGI/II further reduced to < 2.2 (sensitivity 66%, specificity 65.1%) together with PGI < 28 ng/mL (sensitivity 70%, specificity 70%) were the best prediction for gastric cancer. The best cut-off point to diagnose H. pylori infection was anti-H. pylori IgG > 8 U/mL. Multivariate analysis showed that anti-H. pylori IgG > 8 U/mL and PGI/II < 3.1 increased risk for high risk status and PGI/II < 3.1 remained to increase risk for gastric cancer.

The serum diagnosis using PGI/II < 3.1 cut-off value is valuable marker to predict high risk patients for population based massive screening.

Gastric cancer, 1 of the 5 most common causes of cancer death, is associated with a 5-year overall survival rate less than 30%. A minority of cancers occurs as part of syndromic diseases; more than 90% of adenocarcinomas are considered as the ultimate consequence of a longstanding mucosal inflammation. Helicobacter pylori infection is the leading etiology of non-self-limiting gastritis, which may result in atrophy of the gastric mucosa and impaired acid secretion. Gastric atrophy establishes a field of cancerization prone to further molecular and phenotypic changes, possibly resulting in cancer growth. This well-understood natural history provides the clinicopathologic rationale for primary and secondary cancer prevention strategies. A large body of evidence demonstrates that combined primary (H pylori eradication) and secondary (mainly endoscopy) prevention efforts may prevent or limit the progression of gastric oncogenesis. This approach, which is tailored to different country-specific gastric cancer incidence, socioeconomic, and cultural factors, requires that the complementary competences of gastroenterologists, oncologists, and pathologists be amalgamated into a common strategy of health policy.

To present results of the Kyoto Global Consensus Meeting, which was convened to develop global consensus on (1) classification of chronic gastritis and duodenitis, (2) clinical distinction of dyspepsia caused by Helicobacter pylori from functional dyspepsia, (3) appropriate diagnostic assessment of gastritis and (4) when, whom and how to treat H. pylori gastritis.

Twenty-three clinical questions addressing the above-mentioned four domains were drafted for which expert panels were asked to formulate relevant statements. A Delphi method using an anonymous electronic system was adopted to develop the consensus, the level of which was predefined as ≥80%. Final modifications of clinical questions and consensus were achieved at the face-to-face meeting in Kyoto.

All 24 statements for 22 clinical questions after extensive modifications and omission of one clinical question were achieved with a consensus level of >80%. To better organise classification of gastritis and duodenitis based on aetiology, a new classification of gastritis and duodenitis is recommended for the 11th international classification. A new category of H. pylori-associated dyspepsia together with a diagnostic algorithm was proposed. The adoption of grading systems for gastric cancer risk stratification, and modern image-enhancing endoscopy for the diagnosis of gastritis, were recommended. Treatment to eradicate H. pylori infection before preneoplastic changes develop, if feasible, was recommended to minimise the risk of more serious complications of the infection.

A global consensus for gastritis was developed for the first time, which will be the basis for an international classification system and for further research on the subject.

The purpose of our study was to research the applicability of measuring serum pepsinogen I (PG I) and PG I/pepsinogen II (PG II) ratios as screening tests for atrophic gastritis, which is the most important predisposition for stomach cancer.

We measured serum pepsinogen levels in non-specific gastritis, atrophic gastritis and gastric cancer using a radioimmunoassay method. We included in this study 30 healthy control, 30 nonspecific gastritis, 30 atrophic gastritis and 50 gastric cancer cases.

The serum PG I level was statistically higher in the control group and in the patient group with chronic nonspecific gastritis compared to the patient groups with chronic atrophic gastritis and stomach cancer (p<0.05). The best cutoff values for diagnosing stomach cancer using serum PG I and PG I / PG II ratios were found to be <25 ng/ml for PG I and <3.0 for PG I / PG II. The same cut-off values were also most effective for the patients with atrophic gastritis.

Serum pepsinogen screening was shown to be a practical predictor of stomach cancer and atrophic gastritis, the most important predisposing lesion for stomach cancer. Although the diagnosis of stomach cancers localized in the pylorus and cardia via this method is difficult, we believe that the detection of early-stage cancers that develop following chronic atrophic gastritis in particular will be possible, and therefore the morbidity and mortality of stomach cancer will be decreased.

Although the prevalence of gastric cancer (GC) progressively decreased during the last decades, due to improved dietary habit, introduction of food refrigeration and recovered socio-economic level, it still accounts for 10% of the total cancer-related deaths. The best strategy to reduce the mortality for GC is to schedule appropriate screening and surveillance programs, that rises many relevant concerns taking into account its worldwide variability, natural history, diagnostic tools, therapeutic strategies, and cost-effectiveness. Intestinal-type, the most frequent GC histotype, develops through a multistep process triggered by Helicobacter pylori (H. pylori) and progressing from gastritis to atrophy, intestinal metaplasia (IM), and dysplasia. However, the majority of patients infected with H. pylori and carrying premalignant lesions do not develop GC. Therefore, it remains unclear who should be screened, when the screening should be started and how the screening should be performed. It seems reasonable that screening programs should target the general population in eastern countries, at high prevalence of GC and the high-risk subjects in western countries, at low prevalence of GC. As far as concern surveillance, currently, we are lacking of standardized international recommendations and many features have to be defined regarding the optimal diagnostic approach, the patients at higher risk, the best timing and the cost-effectiveness. Anyway, patients with corpus atrophic gastritis, extensive incomplete IM and dysplasia should enter a surveillance program. At present, screening and surveillance programs need further studies to draw worldwide reliable recommendations and evaluate the impact on mortality for GC.

Helicobacter pylori is the main risk-factor for gastric cancer through a cascade from gastritis through atrophic gastritis (AG), intestinal metaplasia (IM), dysplasia (DYS) to malignancy. The presence of these lesions in the general population predicts the gastric cancer incidence in the coming decades. Prevalence data are mostly obtained from serological studies and endoscopy data in symptomatic patients.

To investigate the prevalence of H. pylori infection and its related gastric changes in asymptomatic subjects.

383 Patients undergoing routine colonoscopy were included. All subjects underwent upper GI endoscopy and completed the Gastrointestinal Symptom Rating Scale (GSRS). Biopsies were taken from antrum and corpus.

H. pylori infection was present in 22%. Non-Caucasian subjects had a significantly higher H. pylori prevalence (p < 0.001). AG, IM and DYS were together found in 9.3% of subjects. Subjects with AG, IM or DYS were significantly older (p < 0.001). No differences were found with respect to gender, presence of GI symptoms as scored by GSRS, lifestyle and medication use.

The prevalence of premalignant gastric lesions is considerable in general Western population with increasing age as the main risk factor. One time screening for premalignant lesions at the age of 60 years is a reasonable strategy since the numbers found imply that gastric cancer will remain a prevalent disease.

Chronic atrophic gastritis (CAG) is a precursor of the intestinal type of gastric cancer, the second leading cause of cancer-related death worldwide. GastroPanel is a recently marketed serological kit for the non-invasive diagnosis of CAG, defined by some authors "even more reliable than biopsy histology". The goal of this study was 1) to evaluate the agreement between the serum gastric profile provided by GastroPanel (PGI, PGII, G-17, AbHp) and histology over CAG diagnosis, and 2) to evaluate the prevalence of CAG by means of GastroPanel in a Northern Italian dyspeptic population.

Basal blood samples for GastroPanel parameters evaluation (Biohit Plc, Finland) were collected after an overnight fast from 1387 dyspeptic patients (age range: 18-80 years; F 704). Gastroscopy with two biopsies each of the antrum and corpus was offered to a group of the first 400 consecutive patients (age 18-80 years, F 214) to compare the results of histology and GastroPanel in CAG.

Agreement between GastroPanel and histology for corpus-prevalent CAG was 94%, with a sensitivity and specificity of 80% and 96%, respectively. In our series of 1387 dyspeptic patients, the prevalence of corpus-prevalent CAG, of antral-prevalent CAG and of multifocal CAG (antrum+ corpus) was 10.7%, 3.6% and 2.4%, respectively. Out of the 34 patients with multifocal atrophic gastritis, 12% were under 30 years of age.

GastroPanel is a reliable non-invasive test for diagnosis of CAG and deserves consideration for current use in clinical practice as a valuable diagnostic tool.

Helicobacter pylori infection is linked to the development of gastric cancer. Atrophic body gastritis is considered the first important step in the histogenesis of such neoplasia. H. pylori infection is involved in the induction of atrophic body gastritis, but documentation of H. pylori infection is difficult because of the progressive disappearance of the bacterium. Host-pathogen interactions may be investigated by means of immunoproteomics, which provides global information regarding the host humoral response to H. pylori infection and allows the identification of relevant specific and nonspecific antigens, and can be used for diagnostic or prognostic purposes. In the present review, we describe how several research groups used H. pylori immunoproteomics to investigate highly immunoreactive bacterial antigens related to the development of gastric cancer.

Serological screening for gastric cancer (GC) may reduce mortality. However, optimal serum markers for advanced gastric precursor lesions are lacking.

To evaluate in a case-control study whether serum leptin levels correlate with intestinal metaplasia (IM) and can serve as a tool to identify patients at high risk for GC.

Cases were patients with a previous diagnosis of IM or dysplasia, controls were patients without such a diagnosis. All patients underwent endoscopy. Fasting serum was collected for the measurement of leptin, pepsinogens I/II, gastrin, and Helicobacter pylori. Receiver operating characteristic (ROC) curves and their area under the curve (AUC) were provided to compare serum leptin levels with other serological markers.

One hundred nineteen cases and 98 controls were included. In cases, the median leptin levels were 116.6 pg/mL versus 81.9 pg/mL in controls (p = .01). After adjustment for age, sex and BMI, leptin levels remained higher in cases than in controls (p < .005). In multivariate analysis, male sex (p = .002), age (<0.001), low pepsinogen levels (p = .004) and high leptin levels (p = .04) were independent markers for the presence of IM. In addition, a ROC curve including age, sex and pepsinogen I levels had an AUC of 0.79 (95% CI (0.73-0.85)). Adding serum leptin levels increased the AUC to 0.81 (95% CI (0.75-0.86)).

High leptin levels are associated with an increased risk of IM. Moreover, serum leptin levels are a significant independent marker for the presence of IM. However, in combination with the serological test for pepsinogen I the additional value of serum leptin levels is rather limited.

To assess serologically diagnosed gastric body atrophy (GBA) by histology in a sample of the general population.

GBA is a precursor lesion in gastric cancer. Data on GBA in a primary health care community in the Netherlands have not been reported.

Thirty-four subjects of 997 consecutive adults from a Dutch family practice had serologic GBA, according to hypergastrinemia (>100 ng/L), hypopepsinogenemia A (<17 microg/L), and a low pepsinogen A/C ratio (<1.6). Two years later, 25 subjects of this group, agreed in serologic retesting and gastroscopy with biopsies for histologic assessment according to the Sydney system.

At serologic retesting, 20 of 25 subjects again fulfilled the serologic criteria of GBA. Histologic examination of the corpus biopsies showed advanced GBA in 18 subjects (75%) of 24 (1 subject had no corpus biopsies) and 17 of 19 (89%) subjects with repeated positive serology. After disclosure of serology results, reexamination of the biopsies revealed GBA also in the 2 patients with initially insufficient evidence of GBA, giving a concordance of 100% (19/19). One subject with normal serum gastrin at retesting had both antral and body atrophy giving a concordance between serologic and histologic GBA of 95% (19/20). No adenomatous polyps, tumors, or dysplastic alterations were found.

Identification by serology of asymptomatic patients with advanced GBA in primary care is adequately possible and useful in selecting for endoscopy.

Atrophic gastritis, mainly the consequence of long-standing Helicobacter pylori infection, is linked to the development of gastric cancer. In the case of atrophic gastritis, severity may be mainly related to the lifetime risk of the single patient to develop gastric cancer, mostly in relation to the degree and extension of mucosal damage. As atrophic gastritis is the result of complex multifactorial interactions, the application of artificial neural networks is promising and may be useful for the identification of those patients with atrophic gastritis at higher risk for gastric malignancies. The experience of application of artificial neural networks in atrophic gastritis is still scarce. The available data suggest that these systems may contribute to identify patients with corporal metaplastic atrophic gastritis and to optimize bioptic sampling during gastroscopy.

Although gastric hypochlorhydria is a risk factor for gastroenteritis and for gastric cancer, no reliable, inexpensive, noninvasive test exists for screening or epidemiologic studies. We aimed to evaluate the sensitivity and specificity of the blood quininium resin test (bQRT) for hypochlorhydria, against pH monitoring. Twelve fasting adult volunteers-seven with and five without H. pylori infection-ingested 80 mg/kg of quininium resin twice, once with and once without acid suppression. Gastric pH was monitored for 75 minutes; serum samples were obtained at times 0 and 75 minutes. The bQRT levels were compared to gastric pH, controlling for omeprazole use and H. pylori infection. Subjects with a median recorded pH > or =3.5 were considered hypochlorhydric. Using a bQRT level of 10 as a cutoff for hypochlorhydria, the sensitivity and specificity of the bQRT were 100% and 37.5%, respectively. The bQRT predicted omeprazole use more accurately than pH monitoring. In conclusions, The bQRT has a high sensitivity for hypochlorhydria, making it potentially useful in populations with a high prevalence of hypochlorhydria. In its current formulation, the bQRT's low specificity makes it less useful in low-risk population.

Histology is the gold standard for diagnosis of atrophy but is hampered by observer variation. A reliable method to overcome this issue is morphometric analysis of gastric mucosa. Serum pepsinogens and gastrin have been proposed in the diagnostic work-up of gastric atrophy although diagnostic accuracy of these tests is considered unsatisfactory.

To evaluate the diagnostic accuracy of gastric serum profile in relation both to morphological and morphometric diagnosis of gastric atrophy.

Ninety-four dyspeptic out-patients underwent upper endoscopy and evaluation of serum levels of PGI, PGII and 17-gastrin. Diagnostic accuracy of gastric serum profile was tested by receiver operating characteristic curves and by evaluation of sensitivity and specificity in relation to both histology and morphometric analyses.

As far as concern to histological evaluation, only PGI/PGII ratio showed an acceptable diagnostic accuracy in discrimination of gastric atrophy, while, when morphometric analysis was considered as reference, both serum PGI level and PGI/PGII ratio showed an excellent performance. However, both PGI and PGI/PGII ratio showed low sensitivity and high specificity.

Serological gastric profile corresponds better with the morphometric diagnosis of atrophy, even if, because of the low sensitivity, today this could only be used as screening test of chronic atrophic gastritis.

The relationship between Helicobacter pylori (H. pylori) eradication and atrophic changes in the gastric mucosa has not yet been fully defined. Although studies report a partial restoration of serum pepsinogen I (sPGI) levels after eradication, it is not clear if this finding reflects gastric mucosal healing on a morphological level.

To assess alterations in gastric function after H. pylori eradication on moderate/severe body atrophic gastritis by determination of sPGI levels.

Twenty-three dyspeptic patients, selected from 284 consecutive H. pylori positive patients, with histological features of moderate/severe body atrophic gastritis and sPGI < 25 microg/L (11 men, mean age: 51.8 years, range: 29-79 years), underwent an upper gastrointestinal endoscopy with gastric biopsies and sPGI determination at baseline. All patients underwent eradication therapy. Serum pepsinogen I was measured again after 6 months, and at 1, 2, 3 and 4 years after eradication therapy.

Mean sPGI levels prior to eradication were 11.9 microg/L (range: 4-23 microg/L). Six months after eradication therapy, mean sPGI levels significantly increased to 17.4 microg/L (P = 0.04). At the completion of the study, 4 years after eradication, sPGI levels increased from 17.4 to 32.7 microg/L (P = 0.01). A significant progressive increase in sPGI levels was observed from 6 months to 1 year (17.4 to 23.9 microg/L) and from 1 to 2 years (23.9 to 26.0 microg/L, P = 0.01). Serum pepsinogen I levels higher than the cut-off value of 25 microg/L were observed at various time-points: 6.3% of patients at 6 months (1/16), 33.3% (5/15) at 1 year, 50% (7/14) at 24 months, 66.7% (6/9) at 36 months and 87.5% (7/8) at 4 years.

After H. pylori eradication, subjects with body atrophic gastritis showed long-term improvement of physiological gastric function, reflected by significantly and continually increasing sPGI levels over a 4-year period.

To investigate whether ANNs and LDA could recognize patients with ABG in a database, containing only clinical and biochemical variables, of a pool of patients with and without ABG, by selecting the most predictive variables and by reducing input data to the minimum.

Data was collected from 350 consecutive outpatients (263 with ABG, 87 with non-atrophic gastritis and/or celiac disease [controls]). Structured questionnaires with 22 items (anagraphic, anamnestic, clinical, and biochemical data) were filled out for each patient. All patients underwent gastroscopy with biopsies. ANNs and LDA were applied to recognize patients with ABG. Experiment 1: random selection on 37 variables, experiment 2: optimization process on 30 variables, experiment 3: input data reduction on 8 variables, experiment 4: use of only clinical input data on 5 variables, and experiment 5: use of only serological variables.

In experiment 1, overall accuracies of ANNs and LDA were 96.6% and 94.6%, respectively, for predicting patients with ABG. In experiment 2, ANNs and LDA reached an overall accuracy of 98.8% and 96.8%, respectively. In experiment 3, overall accuracy of ANNs was 98.4%. In experiment 4, overall accuracies of ANNs and LDA were, respectively, 91.3% and 88.6%. In experiment 5, overall accuracies of ANNs and LDA were, respectively, 97.7% and 94.5%.

This preliminary study suggests that advanced statistical methods, not only ANNs, but also LDA, may contribute to better address bioptic sampling during gastroscopy in a subset of patients in whom ABG may be suspected on the basis of aspecific gastrointestinal symptoms or non-digestive disorders.

Apoptosis-modulating approaches offer an attractive opportunity for therapeutic use for many tumors. We investigated the effects of the roots of Coptis japonica var. dissecta (Ranunculaceae) on human gastric cancer cells, SNU-668. The cytotoxicity of Coptis japonica at 100 microg/ml (methanol extract) by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was 13.89 +/- 1.91% of control value. Considering the features by 4,6-diamidino-2-phenylindole (DAPI) staining and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) assay, it was confirmed that the death of SNU-668 cells was due to apoptosis. In the apoptosis-regulating genes, BCL2 expression was diminished out, whereas BAX and CASP3 expressions were increased, compared with control. Furthermore, the activity of caspase3 was significantly increased by Coptis japonica treatment. These results suggest that Coptis japonica could induce apoptotic anticancer effect through caspase3 activation on SNU-668 human gastric cancer cells.

Several tests have been proposed for evaluating dyspeptic symptoms and their relationship to the underlying gastric disease. Serum pepsinogens and gastrin-17 are known to be useful biomarkers for the detection of gastric pathologies.

To evaluate the capability of screening dyspeptic patients in the primary care by analyses of serum pepsinogens I (sPGI) and II (sPGII), gastrin-17 (sG-17) and the IgG anti-Helicobacter pylori antibodies (IgG-Hp).

Three hundred and sixty-two consecutive patients with dyspeptic symptoms (208 females, mean age 50.6 +/- 16 years, range 18-88 years) referred by general practitioners for upper gastrointestinal endoscopy were enrolled. A blood sample was taken from each subject for IgG-Hp, sPGI, sPGII and sG-17 analyses.

Two hundred and eighty-seven patients had a complete screening; of these, 132 resulted positive for Hp infection. Patients with atrophic chronic gastritis showed significantly lower serum pepsinogen I levels and sPGI/sPGII ratio than patients with non-atrophic chronic gastritis. Moreover, by calculating the values of sPGI by sG-17 and sG-17 by sPGII/sPGI, subjects with atrophic chronic gastritis could be distinguished from those with non-atrophic chronic gastritis and from those with normal mucosa, respectively. sG-17 levels were found to be a useful biomarker for the detection of antral atrophic gastritis, while the combination of sPGI, the sPGI/sPGII ratio and sG-17 was found effective in identifying corpus atrophy.

A panel composed of PGI, PGII, G-17 and IgG-Hp could be used as a first approach in the 'test and scope' and/or 'test and treat' strategy in the primary care management of dyspeptic patients.

To investigate the feasibility of combining several serum markers into a valid serum screening tool for gastric cancer, we performed a study evaluating the association between gastric cancer and precancerous conditions and a blood test for gastric acidity (the blood quininium resin test [QRT]) combined with serum pepsinogen levels.

We performed immunoradiometric assays of serum pepsinogen I (PG I), II (PG II) levels, and QRT's in 10 endoscopically normal subjects, in 20 patients with chronic atrophic gastritis, and in 13 patients with biopsy-confirmed gastric adenocarcinoma.

Serum PG I, II levels, I/II ratio were significantly different among normal, gastritis, and cancer patients. Serum PG I/II ratios were much lower in cancer patients. Serum quinine levels by QRT were correlated with PG I/II ratio (rs=0.39, p<0.01). Age was negatively correlated both with PG I/II ratio (rs=-0.58, p<0.01) and serum quinine level (rs=-0.45, p<0.01). The screening using serum PG levels was more valid (sensitivity of 69%, specificity of 77%) than that using QRT alone. The combination of serum PG levels and QRT increased specificity for detecting gastric cancer to 87% without altering sensitivity.

Although blood QRT is a useful addition to other serum screening tests for gastric cancer, these tests alone are not sufficiently accurate as screening tools for gastric cancer.

Gastric cancer remains the second most frequent and lethal malignancy worldwide, with a wide range of incidence rates in different populations. Reducing its incidence is a priority in many high-risk countries, and screening programmes are often advocated as an option. An effective screening programme should have the following characteristics: (i) the disease should be common in the population, otherwise the individual benefit will not offset the risk, cost and inconvenience of screening of the rest of the population; (ii) the diagnostic test(s) used should be safe, simple, inexpensive and reliable; and (iii) effective treatment should be available. With respect to gastric cancer, these conditions are not fulfilled completely in any population and therefore population-based screening does not appear to be a viable approach to the prevention of this neoplasia. In contrast, gastroscopic screening in selected high-risk subjects would seem appropriate. A more effective strategy, particularly in high-incidence populations, could be the widespread screening and treatment for Helicobacter pylori infection. This could result in the virtually complete elimination of chronic gastritis and its associated conditions, including most peptic ulcers, primary gastric B-cell lymphomas and a major portion of gastric epithelial tumours.