Pepsinogen Research Articles

Distinct Clinicopathological Features and Prognosis of Helicobacter pylori Negative Gastric Cancer.

BackgroundWhether the characteristics and prognosis of gastric cancer (GC) are different in patients with and without Helicobacter pylori (HP) remains controversial. The definitions of HP status in patients with atrophic gastritis but negative tests for HP are heterogeneous. We aimed to assess the impact of HP on the prognosis of GC using different definitions.MethodsFrom 1998 Nov to 2011 Jul, five hundred and sixty-seven consecutive patients with GC were included. HP status was determined by serology and histology. Patients with any positive test were defined as HP infection. Patients without HP infection whose serum pepsinogen (PG) I <70 ng/dl and PG I/II ratio < 3.0 were defined as atrophic gastritis and they were categorized into model 1: HP positive; model 2: HP negative; and model 3: exclusion of these patients.ResultsWe found four characteristics of HP negative GC in comparison to HP positive GC: (1) higher proportion of the proximal tumor location (24.0%, P = 0.004), (2) more diffuse histologic type (56.1%, p = 0.008), (3) younger disease onset (58.02 years, p = 0.008) and (4) more stage IV disease (40.6%, p = 0.03). Patients with negative HP had worse overall survival (24.0% vs. 35.8%, p = 0.035). In Cox regression models, the negative HP status is an independent poor prognostic factor (HR: 1.34, CI:1.04–1.71, p = 0.019) in model 1, especially in stage I, II and III patients (HR: 1.62; CI:1.05–2.51,p = 0.026).ConclusionWe found the distinct characteristics of HP negative GC. The prognosis of HP negative GC was poor.

A multi-center clinical research of diagnostic value of serum gastrin-17 combined with pepsinogen for gastric cancer

Objective To evaluate the diagnostic value of gastrin-17(G-17) and pepsinogen(PG) for gastric cancer. Methods A multicenter cross-sectional study of patients with continuous stomach discomfort from four centers including Changhai Hospital Affiliated to Second Military Medical University, the First Hospital Affiliated to Anhui Medical University, Qinghai Provincial People′s Hospital and the First Hospital Affiliated to Zhejiang University of Chinese Medicine from May 2014 to September 2015 was conducted. Before gastroscopy, fasting serum gatrin-17 and pepsinogen were analyzed by enzyme-linked immunosorbent assay(ELISA). The efficacy of G-17 and PG were evaluated according to endoscopic and pathological results. Results Based on the results of the pathological diagnosis, 1 122 cases were enrolled and divided into chronic atrophic gastritis group(548 cases), chronic non-atrophic gastritis group(370 cases), and gastric cancer group(204 cases). Serum G-17 and PGⅡ levels significantly increased(P 7 pmol/L and PGR 7 pmol/L and PGⅡ>10 μg/L was regarded as the cut-off value, the sensitivity, specificity, accuracy, positive predictive value and negative predictive value were 48.04%, 79.74%, 73.98%, 34.51% and 87.35% respectively. If PGR 10 μg/L was regarded as the cut-off value, the sensitivity, specificity, accuracy, positive predictive value and negative predictive value were 33.82%, 84.86%, 75.58%, 33.17% and 85.23% respectively. Based on logistic regression analysis of the independent variables of high serum G-17 value(>7 pmol/L), low serum PGR value( 10 μg/L), their OR value were 2.592, 2.237 and 1.864 respectively, and high serum G-17 value showed the highest risk of gastric cancer. Conclusion High serum G-17 and PGⅡ, low PGR are indicators of gastric cancer. Combination of G-17 and PGR has the best diagnostic value for gastric cacer. Gastric cancer can be screened in large scale by combining G-17 and PGR in order to improve the early diagnostic rate of gastric cancer and reduce the mortality of gastric cancer in our country. Key words: Stomach neoplasms; Diagnosis; Multicenter study; Pepsinogens; Gastrin-17

The Impact of Gastric Atrophy on the Incidence of Diabetes

Gastric atrophy results in lower plasma ghrelin, higher gastrin secretion, a change in gut microbiota, and altered dietary nutrient absorption, which may be associated with the incidence of diabetes. Helicobacter pylori (H. pylori) infection is a major cause of gastric atrophy and is associated with diabetes in some reports. Since there is no study which investigates the impact of gastric atrophy on diabetes, we conduct a prospective cohort study to examine the relationship between H. pylori infection, gastric atrophy, and incident diabetes. In this study, subjects with gastric atrophy had a lower risk of incident diabetes, compared to those without gastric atrophy. The extent of gastric atrophy, measured by serum pepsinogen (PG) I/II ratio, was correlated with age, H. pylori IgG titer, HOMA2-IR, and HOMA2%B. When gastric atrophy is more extensive, presented as a lower serum PG I/II ratio, the risk of incident diabetes is lower. On the other hand, there was no significant association between H. pylori infection and the incidence of diabetes. In conclusion, the presence and the extent of gastric atrophy, but not H. pylori infection, are associated with incident diabetes. Further studies are needed to investigate the detailed mechanisms and the potential applications of the findings to guide diabetes screening and treatment strategies.

Discrepant impacts of age and gender factors on serum pepsinogens and gastrin-17 levels

Background: To explore the effect of age and gender on serum pepsinogen I (PGI), pepsinogen II (PGII), and gastrin-17 (G-17) levels. Methods: We recruited 2,732 people who underwent physical examination in our hospital and detected their serum PGI, PGII, and G-17 levels by enzyme-linked immunosorbent assay (ELISA). We applied one-way ANOVA, Student’s t-test, and Spearman correlation, one way analysis of variance, Tukey test, and non-parametric 95% percentile method for statistical analysis. Results: In both males and females, PGI, PGII and G-17 were positively correlated with age. Males had significantly higher PGI and PGII than females, while G-17 was not affected by gender. Besides, we established the gender and age specific reference intervals for PGs and G-17. Conclusions: Both age and gender should be taken into consideration when interpreting serum PGI, PGII, and G-17 results.

Link between Serum Pepsinogen Concentrations and Upper Gastrointestinal Endoscopic Findings.

The serum pepsinogen (PG) assay findings are correlated with the status of Helicobacter pylori infection, but there are controversies on the link with upper gastrointestinal (UGI) endoscopic findings. The aim of this study was to determine the significance of a serum PG assay for correlating with endoscopic findings in H. pylori-seroprevalent adult population. Korean adults who visited for a health check-up were included consecutively. Subjects after gastrectomy or H. pylori eradication were excluded. After completing the serum PG assay and anti-H. pylori immunoglobulin G (IgG) titer on the same day of UGI endoscopy, subjects with equivocal serology test finding or gastric neoplasm were excluded. Of the 4,830 included subjects, 3,116 (64.5%) were seropositive for H. pylori. Seropositive finding was related to high serum PG I (P < 0.001) and PG II (P < 0.001) concentrations, low PG I/II ratio (P < 0.001), old age (P < 0.001), and male gender (P = 0.006). After adjusting age and gender, the serum PG I and II concentrations were positively correlated with the presence of nodular gastritis (NG) (all P = 0.003). The serum PG I was positively correlated with gastric ulcer (P = 0.003), and it was correlated with duodenal ulcer in seropositive subjects (P = 0.008). The PG I/II ratio was positively correlated with erosive esophagitis, while it was inversely related to chronic atrophic gastritis and metaplastic gastritis (all P < 0.001). Our findings suggest that the serum PG assay finding correlates well with the UGI endoscopic finding. A higher serum PG concentration in subjects with NG and peptic ulcer disease suggests that endoscopic findings reflect gastric secreting ability.

Serological Changes after Equivocal Helicobacter pylori-serology Test Findings Dependent on Gastric Secreting Ability

The serum anti-Helicobacter pylori (H. pylori) immunoglobulin G (IgG) and serum pepsinogen (PG) assays are widely used to screen for gastric cancer. An equivocal serology test finding indicates IgG titer between the positive and negative test findings. This study aims to evaluate the long-term follow-up result after an equivocal test finding on the serum anti-H. pylori IgG assay. Koreans aged 18 years or older with an equivocal serum anti-H. pylori IgG assay finding were included. Subjects were excluded if they did not undergo H. pylori serology test, serum PG assay, and upper gastrointestinal (UGI) endoscopy on the same day at our center. The annual test findings were followed-up using the same methods. Of the 7,178 subjects who underwent the serum assays and UGI endoscopy on the same day, 274 (3.8%) subjects showed an equivocal H. pylori serology test finding. Of the 98 subjects who were followed-up, 58 (59.2%) showed seropositive finding at the mean follow-up period of 30.6±12.4 months. Subjects with seroconversion showed a higher initial serum PG I (p=0.023) and PG II (p=0.036) levels than those without seroconversion. An equivocal H. pylori serology test finding was not rare (3.8%) in Korean adults, and 60% of equivocal subjects showed seroconversion within 3 years. Higher seroconversion rates in subjects with high PG I and PG II levels suggest that intact gastric secreting ability plays a role in the survival of H. pylori. Therefore, equivocal subjects with increased serum PG levels should be considered as potential seropositive subjects.

胃がんリスク検診により発見された&lt;i&gt;H. pylori&lt;/i&gt;初感染の1例

A 69-year-old woman was referred to us because of abnormally high serum pepsinogen (PG) levels in the ABC method (blood test for gastric cancer screening) done in April 2016, which resulted in group A. EGD performed in May 2016 revealed diffuse redness and mucosal swelling, indicating HP-associated gastritis, although the endoscopic findings in 2014 had indicated a HP-negative gastric mucosa. A rapid urease test was positive. From April to June 2016, serum PGI levels decreased, and serum HP antibody levels increased and changed from negative to positive. Thus, the initial HP infection was found by abnormally high PG levels and then converted to chronic persistent infection. The ABC method should be evaluated not only by the groups but also by serum PG and HP antibody levels, as well as endoscopic findings.

Serological Biomarker Panel (GastroPanel®): A Test for Non-Invasive Diagnosis of Dyspeptic Symptoms and for Comprehensive Detection of Helicobacter pylori Infection

The two major risk factors of Gastric Cancer (GC) are Helicobacter pylori (HP) infection and Atrophic Gastritis (AG) It is currently possible to diagnose HP-infection and AG by using serological testing with a panel of biomarkers (GastroPanel®, Biohit Oyj, Finland): Pepsinogen I (PGI), Pepsinogen II (PGII), Gastrin-17 (G-17) and HP-antibodies. In this review, an introduction is made to the GastroPanel® test as the first non-invasive diagnostic tool for: i) Dyspeptic symptoms, ii) Screening of asymptomatic subjects for the risks of GC, iii) A comprehensive diagnosis of HP-infection. GastroPanel® test is based on stomach physiology both in health and disease. Accordingly, pepsinogen levels and their ratio is decreased in corpus atrophy (AGC), accompanied by elevated G-17b (basal) G-17b level also sensitively responds to gastric acid output, being low with high acid output and high when the stomach is acid-free (due to PPI-treatment or AGC) In Antrum Atrophy (AGA), G-17b is low and, importantly, does not respond to protein stimulation (G-17s), because the G-cells are disappeared. The results of GastroPanel® test are interpreted by a special software (GastroSoft®) identifying 8 diagnostic marker profiles. Of those, four (profiles 1, 2, 3, and 8) represent purely functional disorders (of acid output), while three others specify structural abnormalities (profiles 5, 6, and 7 for AGC, AGA, and AGpan, respectively) the remaining (profile 4) is typical to HPinfection, with three possible outcomes: a) Active HPinfection, b) Successful eradication, and c) Failed eradication. GastroPanel® test has been validated in both clinical and screening settings. The entire published literature was subjected to systematic review and meta-analysis, including 27 eligible studies that comprise almost 9.000 patients. GastroPanel® was shown to perform better in diagnosis of AGC than AGA, with 70.2% vs. 51.6% pooled SE, and 93.9% vs. 84.1% pooled SP, respectively. This first meta-analysis corroborates the recently launched statement of 16 international experts, advocating the use of this non-invasive serological test as the first-line diagnostic tool for dyspeptic symptoms and for screening of the risks of GC among asymptomatic subjects. The two most commonly used HP tests (UBT and SAT) are prone to false-negative results in conditions with decreased bacterial loads in the stomach: 1) Use of PPI medication; 2) Use of antibiotics; 3) Bleeding peptic ulcer; 4) AG; 5) GC; 6) MALT lymphoma, and 7) Partial gastrostomy. False-positive results do occur in cases where urease-producing bacterial species are colonizing an acid-free stomach (AG or PPI users) it is mandatory that these serious limitations in the use of UBT and SAT are properly acknowledged while these two HP tests are being promoted. Given that this bacteria is the single most important risk factor of GC, it is time to move a step forward also in the diagnosis of HP-infections, and start using the test (GastroPanel®) that is: i) Free from the shortcoming of the conventional HP tests, and ii) Provides an added value by detecting also the other key risk factor of GC, i.e., AG with all its potentially serious clinical sequels.

Characteristics of gastric cancer in negative test of serum anti-Helicobacter pylori antibody and pepsinogen test: a multicenter study.

The serological risk prediction system combines the pepsinogen test and anti-Helicobacter pylori (H. pylori) antibody determination. In this system, chronic atrophic gastritis (CAG) is diagnosed using the pepsinogen test. Patients who are H. pylori negative and pepsinogen negative are classified into group A, are assumed to be H. pylori uninfected, and are at an extremely low risk for gastric cancer. However, gastric cancers are detected in this group. The aim of this study is to clarify the clinicopathological status of group A patients with gastric cancer. A total of 109 gastric cancer patients classified as group A were enrolled in a multicenter study. Group A patients were divided into two subgroups: group AN (H. pylori uninfected) and group AP (H. pylori infected). They were compared to 183 H. pylori-infected gastric cancer patients who were not in group A. Of the 109 patients, only 7 were classified as group AN; the other 102 were classified as group AP. The clinicopathological features of group AP included older age, predominantly differentiated type cancer, endoscopically visualized CAG, and pepsinogen (PG) I/II ratio lower than that of group AN. In group AN, the depressed type was dominant, and the PG I/II ratio was higher than in those gastric cancer patients who were infected with H. pylori. Patients in group AP had CAG, and their gastric cancers were similar to those of H. pylori-eradicated patients. Concerning the recent ABC classification system, advanced decision criteria should be proposed to decrease the false-negative evaluation of gastric cancer risk.

Severity of Gastric Mucosal Atrophy Is the Major Determinant of Plasma Ghrelin Level in Hemodialysis Patients

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.

Gastric cancer - clinical and epidemiological aspects.

Gastric cancer (GC) ranks fifth for cancer incidence and second for cancer deaths. Epidemiological data showed that survivors of Hodgkin's lymphoma and patients with pernicious anemia etiologically linked to autoimmune gastritis are at increased risk of GC. Screening of patients with autoimmune thyroid disease by means of pepsinogen (PG) I and PG I/II detected autoimmune gastritis with oxyntic gastric atrophy in one of four patients and may be recommended for GC prevention purposes. The International Agency for Research on Cancer reported a positive association between consumption of processed meet and increased GC risk. A new GC risk prediction model based on biological markers, age, gender, smoking status, family history of GC, and consumption of highly salted food showed good predictive performance, and might prompt individuals to modify their lifestyle habits, attend regular check-up visits or participate in screening programs. A novel GC classification based on gene expression of primary resected cancers correlated with clinicopathological features. Noncoding RNA for GC screening remains the focus of multiple studies. Patients with early GC undergoing endoscopic resection are more likely to develop metachronous lesions than patients undergoing surgery and endoscopic surveillance is warranted in this special cohort. The addition of gastrectomy to chemotherapy did not improve survival of patients with advanced GC and a single noncurable factor. Apatinib, a novel oral vascular endothelial growth factor receptor 2 tyrosine kinase inhibitor, improved the median overall survival of patients with advanced GC and progressive disease after two or more lines of prior chemotherapy of nearly 3months.

Serum Pepsinogen Levels Are Correlated With Age, Sex and the Level of Helicobacter pylori Infection in Healthy Individuals

BackgroundTo explore the relationship between age, sex, the level of Helicobacter pylori (HP) infection and serum pepsinogen (PG) in healthy people undergoing a medical examination. MethodsA total of 6,596 “healthy” individuals undergoing a medical examination were selected as subjects in this study. The concentrations of serum pepsinogen I (PGI) and serum pepsinogen II (PGII) were tested for each of the subjects using time-resolved fluorescence immunoassay characterized with high sensitivity and wide measuring range. The infection ratio and level of HP were tested using a 13C-urea breath test to analyze the relationship between age, sex, HP infection, and serum PGs. ResultsThe PGI, PGII and PGI-to-PGII ratio (x¯±S) were higher in males than in females. The serum PGI and PGII levels gradually increased with age. HP infection rate was 48.83%, and the serum PGI, PGII and PGI-to-PGII ratio (x¯±S) were 187.05 ± 73.50µg/L, 18.09 ± 8.68µg/L and 11.67 ± 5.44, respectively in the HP-positive group and 150.39 ± 67.04µg/L, 11.50 ± 7.45µg/L and 15.67 ± 8.19, respectively in the HP-negative group. There was significant difference in the detection rate of an abnormal PG between the 2 groups as with the worsening of HP infection, 13C-urea breath test and serum PGI and PGII levels increased, but the PGI-to-PGII ratio decreased significantly. ConclusionsSerum PGI and PGII levels were correlated with age, sex and the level of HP infection. Therefore, the influencing factors of age, sex and the level of HP infection should be considered when screening stomach diseases using PG.

Pepsinogens to Distinguish Patients With Gastric Intestinal Metaplasia and Helicobacter pylori Infection Among Populations at Risk for Gastric Cancer.

Objectives:The objectives of this study were to investigate the serum pepsinogen test for the prediction of OLGIM (Operative Link on Gastric Intestinal Metaplasia Assessment) stages in first-degree relatives (FDR-GC) of patients with gastric cancer (GC) and autoimmune chronic atrophic gastritis (ACAG).Methods:In 67 consecutive patients with ACAG, 82 FDR-GC, and 53 controls (CTRL) without gastric disease (confirmed by biopsy), serum levels of pepsinogen 1 (PG1), pepsinogen 2 (PG2), G17, and the PG1/2 ratio were assessed by enzyme-linked immunosorbent assay kit. All ACAG patients had positive antiparietal cell antibody levels, estimated by indirect immunofluorescence. Biopsies taken in duplicate from the antrum, corpus, and fundus were stained with Giemsa for Helicobacter pylori detection. Endoscopic detection of metaplasia was confirmed by histological diagnosis. Histological classification of OLGIM stages was applied by using the criteria of severity and topography of intestinal metaplasia (IM).Results:The highest discrimination capacity for distinguishing ACAG from other groups of patients was the gastrin G17 test. The lowest mean for PG1 and PG2 serum levels was found in ACAG. In multivariate analysis by age, PG1 and PG1/PG2 were independent prognostic factors for metaplasia, and PG2 also for the presence of a histological H. pylori infection. The serum PG1 level was significantly lower in individuals with IM at OLGIM stage >2 than in those with IM at OLGIM stage <2, resulting in a useful method for the prediction of OLGIM stage. With the inclusion of patient age at diagnosis in the prediction of ≥2 vs. 0–1 OLGIM stages, the receiver operating characteristic (ROC) curve at 47.9 ng/ml PG1 level reached a significant area under the curve (AUC) value (0.978, P<0.001). We also observed a slight difference in PG2 serum levels between histological H. pylori-positive and H. pylori-negative subjects (ROC AUC: 0.599).Conclusions:This study demonstrated an important increase in gastrin G17 serum level in autoimmune gastritis. PG1 serum level corrected by patient age can be used in the management of patients at risk for GC with a high predicted probability of having an OLGIM stage ≥2. Using a cutoff of 47.9 ng/ml, PG1 testing in FDR-GC and ACAG patients had a sensitivity of 95.83% and a specificity of 93.37. Although these results could be validated in a prospective study, the known importance of higher OLGIM stages in increasing the risk of GC development supports the rationale of proposing PG1 algorithm as a diagnostic tool for the selection of high-risk FDR-GC and ACAG patients at high-risk stages for subsequent detailed endoscopic examination to detect dysplasia and asymptomatic GC. In addition, serum PG1 and PG2 levels could stratify patients based on both H. pylori infection and OLGIM risk in consideration of the increased acknowledge regarding the role of H. pylori in the progression of gastritis to GC.

Actual Status of Involvement of Helicobacter pylori Infection That Developed Gastric Cancer from Group A of ABC (D) Stratification - Study of Early Gastric Cancer Cases That Underwent Endoscopic Submucosal Dissection

Background/Aims: Patients who are Helicobacter pylori antibody negative and have normal pepsinogen (PG) levels (group A of ABC (D) stratification) are considered unlikely to develop gastric cancer. This study aimed to clarify the involvement (uninfection, present infection or previous infection) of H. pylori in group A patients with early gastric cancer who underwent endoscopic submucosal dissection (ESD) by examining their background gastric mucosa endoscopically and histologically. Methods: This study included 166 patients with gastric cancer who were treated by ESD. Patients were classified according to PG levels and H. pylori antibody titers. Three biopsies (greater curvature of the antrum, lesser curvature of the middle corpus and greater curvature of the middle corpus) from group A were histologically analyzed and compared with those of groups B, C, D and after eradication). Results: In group A (34 patients), 32 patients had endoscopic atrophy (group A′). Histological neutrophil activity, chronic inflammation and atrophy scores were lower in group A′ than in other groups. Group A′ scores were similar to those of the after eradication group. Conclusion: Most of the group A patients with early gastric cancer were not uninfected with H. pylori, but had previous infections, thus carrying carcinogenic risk.

Immunomodulatory Effect of H. Pylori CagA Genotype and Gastric Hormones On Gastric Versus Inflammatory Cells Fas Gene Expression in Iraqi Patients with Gastroduodenal Disorders.

AIM:To evaluate the Immunomodulatory effects of CagA expression; pepsinogen I, II & gastrin-17 on PMNs and lymphocytes Fas expression in inflammatory and gastric cells; demographic distribution of Fas molecule in gastric tissue and inflammatory cells.METHODS:Gastroduodenal biopsies were taken from 80 patients for histopathology and H. pylori diagnosis. Serum samples were used for evaluation of pepsinogen I (PGI); (PGII); gastrin-17 (G-17).RESULTS:Significant difference (p < 0.001) in lymphocytes & PMNs Fas expression; epithelial & lamina propria Fas localization among H. pylori associated gastric disorders. No correlation between grade of lymphocytes & PMNs Fas expression in gastric epithelia; lamina propria and types of gastric disorder. Significant difference (p < 0.001) in total gastric Fas expression, epithelial Fas; lamina propria and gastric gland Fas expression according to CagA, PGI; PGII; PGI/PGII; Gastrin-17. Total gastric Fas expression has significant correlation with CagA, PGII levels. Gastric epithelial and gastric lamina propria Fas expression have significant correlation with CagA, PGI; PGII levels. Significant difference (p < 0.001) was found in lymphocytes & PMNs Fas expression; epithelial & lamina propria localization of lymphocytes & PMNs Fas expression according to CagA, PGI; PGII; PGI/PGII; Gastrin-17. Lymphocytes Fas expression have correlation with PGI, PGII, PGI/PGII. PMNs Fas expression have correlation with PGI, PGII.CONCLUSION:Fas gene expression and localization on gastric and inflammatory cells affected directly by H. pylori CagA and indirectly by gastric hormones. This contributes to progression of various gastric disorders according to severity of CagA induced gastric pathology and gastric hormones disturbance throughout the course of infection and disease.

Comparison of serum trefoil factor 3 with the pepsinogen test for the screening of diffuse-type gastric cancer

Emerging data show that serum trefoil factor 3 (TFF3) alone and combined with the serum pepsinogen (PG) test can increase the diagnostic yield of gastric cancer. We aimed to evaluate the diagnostic value of serum TFF3 for the screening of gastric cancer in Korean patients, especially for the screening of the diffuse type of gastric cancer, and compared TFF3 to the serum PG test. We enrolled 25 healthy controls and 79 subjects with gastric cancer who underwent endoscopic resection or surgery from June 2006 to June 2015. Data about age, sex, histological type according to the Lauren classification, stage of gastric cancer, and status of H. pylori were collected. Serum levels of PG I and PG II were measured by the latex-enhanced turbidimetric immunoassay, and serum TFF3 levels were measured by enzyme-linked immunosorbent assay. The optimal cutoff value of serum TFF3 was ≥8.9ng/mL to diagnose gastric cancer, with 73.4% sensitivity and 92.0% specificity, which were higher than those of the serum PG I/II ratio, with 69.6% sensitivity and 68.0% specificity. The optimal sensitivity and specificity of serum TFF3 for the diagnosis of diffuse-type gastric cancer were 68.0 and 92.0%, respectively, which were lower than those for the diagnosis of intestinal-type gastric cancer (75.6 and 100%, respectively). Serum TFF3 is a more stable and useful marker than the serum PG test for the screening of gastric cancer in Korean patients. Serum TFF3 showed good diagnostic power in detecting both intestinal- and diffuse-type gastric cancer although it showed decreased power in diffuse type.

Serum pepsinogen levels can quantify the risk of development of metachronous gastric cancer after endoscopic resection.

We have previously reported that serum pepsinogen (PG) can quantify the level of gastric mucosal atrophy, and that H. pylori eradication reduces cancer development in subjects with mild atrophy identified by serum PG levels. The aim of this study was to elucidate the predictive ability of serum PG levels for the development of metachronous gastric cancer (MGC) after endoscopic resection (ER) of primary cancer in association with H. pylori eradication. A retrospective chart review was performed, and 330 patients who underwent ER for initial early gastric cancer were enrolled. Presence or absence of H. pylori, serum PG levels, and endoscopic atrophy at ER were evaluated. H. pylori eradication was performed at the patient's request after ER. The incidence of MGC in these patients was analyzed. Of 330 patients, 47 developed MGC. Endoscopic extensive atrophy was observed more frequently in patients with MGC (p = 0.001). Although PG I or PG II alone did not significantly differ according to development of MGC, the proportion of PG I/II ≤ 3.0, which is one of the criteria of PG test-positive, was significantly higher in patients with MGC (83 vs. 69%, p = 0.04). H. pylori eradication after ER did not affect MGC development (p = 0.2). On multivariate analysis, serum PG I/II ratio ≤ 3.3 was significantly associated with the development of MGC (hazard ratio: 3.66, 95% confidence interval: 1.47-12.25, p = 0.004). The risk of MGC after ER could be quantitatively predicted by the PG I/II ratio regardless of H. pylori status.

In Situ Nick End Labeling as a Molecular Immunopathological Indicator for the Severity of DNA Fragmentation and Gastroduodenal Tissue Damage among H. Pylori Cag A&lt;sup&gt;Positive&lt;/sup&gt; Patients

Background and Objective: The aim is to determine the correlation between gastric Apoptotic Index (AI), inflammatory cells AI; H. pylori CagA; Gastric secretions; and other proposed factors that may induce apoptosis and subsequently induce different gastric lesions. Methodology: Gastroduodenal biopsies taken from 80 patients for histopathology and H. pylori diagnosis. Cag A and DNA fragmentation detected by in situ hybridization Serum samples used for evaluation of Serum pepsinogen I (PGI); II (PGII; Gastrin-17 (G-17) . Findings: Significant difference between gastric tissue (AI), inflammatory cells; inflammatory cells versus gastric tissue AI; CagA positivity among gastric disorders (p value = 0.022). Cag A correlated with gastric AI and inflammatory cells AI. Significant difference in Inflammatory Cells AI among Cag Apositive versus CagA negative cases (p value = 0.002). Significant difference in AI between gastric tissue and Inflammatory Cells among Cag A positive (p value = 0.000) with inverse correlation (p value = 0.014). Gastric AI and Inflammatory cells AI Inversely correlated with PGI/PGII level and CagA positivity. Marginal inverse correlation between gastric AI, Gastrin17 level and CagA positivity was reported (p value = 0.056). Inflammatory cells AI correlated with PMNs grade and CagA positivity (p = 0.044). Gastric cells AI correlated with PMNs grade (p = 0.001). Gastric AI and inflammatory cells AI correlated with age. Gastric AI and inflammatory cells AI inversely correlated with gender. Significant difference in gastric AI; inflammatory cells AI and usage of PPIs; NSAID usage; smoking, drinking of tap water. Marginal inverse correlation between NSAID usage and gastric AI (p = 0.000), inflammatory cells AI (p = 0.001). Conclusion: Cag A correlated with AI among different gastro duodenal nonmalignant disorders. Inverse correlation between AI and PGI/PGII level; gastric AI and Gastrin17 level. AI correlated with PMNs grade; age and Cag A positivity. AI not correlated with PPIs, smoking, tap water. Inflammatory cells AI Inversely correlated with Gender.

Oxyntic gastric atrophy in Helicobacter pylori gastritis is distinct from autoimmune gastritis

AimTo assess characteristics of oxyntic gastric atrophy (OGA) in autoimmune gastritis (AIG) compared with OGA as a consequence of Helicobacter pylori infection.MethodsPatients undergoing oesophagogastroduodenoscopy from July 2011 to October 2014...

Does the antibody production ability affect the serum anti-Helicobacter pylori IgG titer?

To investigate the relationship between serum titers of anti-Helicobacter pylori (H. pylori) immunoglobulin G (IgG) and hepatitis B virus surface antibody (HBsAb). Korean adults were included whose samples had positive Giemsa staining on endoscopic biopsy and were studied in the hepatitis B virus surface antigen (HBsAg)/HBsAb serologic assay, pepsinogen (PG) assay, and H. pylori serologic test on the same day. Subjects were excluded if they were positive for HBsAg, had a recent history of medication, or had other medical condition(s). We analyzed the effects of the following factors on serum titers of HBsAb and the anti-H. pylori IgG: Age, density of H. pylori infiltration in biopsy samples, serum concentrations of PG I and PG II, PG I/II ratio, and white blood cell count. Of 111 included subjects, 74 (66.7%) exhibited a positive HBsAb finding. The serum anti-H. pylori IgG titer did not correlate with the serum HBsAb titer (P = 0.185); however, it correlated with the degree of H. pylori infiltration on gastric biopsy (P < 0.001) and serum PG II concentration (P = 0.042). According to the density of H. pylori infiltration on gastric biopsy, subjects could be subdivided into those with a marked (median: 3.95, range 0.82-4.00) (P = 0.458), moderate (median: 3.37, range 1.86-4.00), and mild H. pylori infiltrations (median: 2.39, range 0.36-4.00) (P < 0.001). Subjects with a marked H. pylori infiltration on gastric biopsy had the highest serological titer, whereas in subjects with moderate and mild H. pylori infiltrations titers were correspondingly lower (P < 0.001). After the successful eradication, significant decreases of the degree of H. pylori infiltration (P < 0.001), serum anti-H. pylori IgG titer (P < 0.001), and serum concentrations of PG I (P = 0.028) and PG II (P = 0.028) were observed. The anti-H. pylori IgG assay can be used to estimate the burden of bacteria in immunocompetent hosts with H. pylori infection, regardless of the HBsAb titer after HBV vaccination.