gastrin-17 and Helicobacter-Infections

Upper-GI diseases are one of the most relevant issue in primary care. Nowadays they are still responsible for about 100 million ambulatory care visits only in the US. The diagnosis of almost every upper-GI condition is still deputed to invasive tests such as upper gastrointestinal endoscopy, gastroesophageal manometry or radiography. The possibility of analysing serum markers like Pepsinogens I and II, produced by gastric mucosa, in order to assess the functional characteristics of the upper GI tract has spread itself since the 80's especially in the diagnosis of peptic ulcer. The discovery of Helicobacter pylori by Marshall and Warren in 1983 and the scientific consecration of its role in the pathogenesis of gastric cancer and peptic ulcer (crystallized in Peleo Correa's Cascade, 1992), led to an increase importance of non-invasive tests, raising the attention towards the assessment of both immunoglobulins anti-H.p. and Gastrin hormone produced by antral G cells, as an implementation of the panel of gastric markers. This narrative review aims to analyze the huge landscape of non-invasive tests for diagnosis of GI diseases, studying the literature of the recent years.

Topics: Antibodies, Bacterial; Biomarkers; Diagnostic Techniques, Digestive System; Dyspepsia; Endoscopy, Gastrointestinal; Esophageal Diseases; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Pepsinogens; Stomach Diseases

The combination of pepsinogen, gastrin-17 and anti-H. pylori antibodies serological assays (panel test) is a non-invasive tool for the diagnosis of atrophic gastritis. However, the diagnostic reliability of this test is still uncertain.. To assess the diagnostic performance of the serum panel test for the diagnosis of atrophic gastritis.. Medline via PubMed, Embase, Scopus, Cochrane Library databases and abstracts of international conferences proceedings were searched from January 1995 to December 2016 using the primary keywords "pepsinogens," "gastrin," "atrophic gastritis," "gastric precancerous lesions." Studies were included if they assessed the accuracy of the serum panel test for the diagnosis of atrophic gastritis using histology according to the updated Sydney System as reference standard.. Twenty studies with a total of 4241 subjects assessed the performance of serum panel test for the diagnosis of atrophic gastritis regardless of the site in the stomach. The summary sensitivity was 74.7% (95% confidence interval (CI), 62.0-84.3) and the specificity was 95.6% (95%CI, 92.6-97.4). With a prevalence of atrophic gastritis of 27% (median prevalence across the studies), the negative predictive value was 91%. Few studies with small sample size assessed the performance of the test in detecting the site of atrophic gastritis.. The combination of pepsinogen, gastrin-17 and anti-H. pylori antibodies serological assays appears to be a reliable tool for the diagnosis of atrophic gastritis. This test may be used for screening subjects or populations at high risk of gastric cancer for atrophic gastritis; however, a cost-effectiveness analysis is needed.

Topics: Cost-Benefit Analysis; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Hematologic Tests; Humans; Pepsinogen A; Prevalence; Reproducibility of Results; Sensitivity and Specificity; Stomach Neoplasms

Atrophic gastritis (AG) results most often from Helicobacter pylori (H. pylori) infection. AG is the most important single risk condition for gastric cancer that often leads to an acid-free or hypochlorhydric stomach. In the present paper, we suggest a rationale for noninvasive screening of AG with stomach-specific biomarkers.. The paper summarizes a set of data on application of the biomarkers and describes how the test results could be interpreted in practice.. In AG of the gastric corpus and fundus, the plasma levels of pepsinogen I and/or the pepsinogen I/pepsinogen II ratio are always low. The fasting level of gastrin-17 is high in AG limited to the corpus and fundus, but low or non-elevated if the AG occurs in both antrum and corpus. A low fasting level of G-17 is a sign of antral AG or indicates high intragastric acidity. Differentiation between antral AG and high intragastric acidity can be done by assaying the plasma G-17 before and after protein stimulation, or before and after administration of the proton pump inhibitors (PPI). Amidated G-17 will rise if the antral mucosa is normal in structure. H. pylori antibodies are a reliable indicator of helicobacter infection, even in patients with AG and hypochlorhydria.. Stomach-specific biomarkers provide information about the stomach health and about the function of stomach mucosa and are a noninvasive tool for diagnosis and screening of AG and acid-free stomach.

Topics: Achlorhydria; Antibodies, Bacterial; Biomarkers; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Mass Screening; Pepsinogen A; Pepsinogen C; Stomach Neoplasms; Vitamin B 12

Topics: Biomarkers; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Pepsinogens; Risk Factors; Stomach Neoplasms

On the basis of the levels of serum pepsinogen I (S-PGI) and gastrin-17 (S-G-17) as well as Helicobacter pylori - antibodies assayed from a blood sample it is possible to establish with high sensitivity and specificity whether the patient has gastritis, whether the gastritis is atrophic or not and in which part of the stomach the atrophic changes are located. The test enables the identification of patients whose risk of gastric cancer, of the consequences of vitamin B12 deficiency (e.g. elevated levels of homocysteine) or of peptic ulcer is considerably increased and who can then undergo gastroscopy. It also facilitates the diagnosis of non-atrophic Helicobacter gastritis enabling treatment before endoscopy.

Topics: Finland; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Humans; Pepsinogen A; Peptic Ulcer; Stomach Neoplasms; Vitamin B 12 Deficiency

Develop a program to identify, treat, and prevent severe atrophic gastritis to reduce gastric cancer incidence and mortality.. In total, 2,847 people aged > 40 years old underwent serological noninvasive screening for atrophic gastritis by identifying postprandial gastrin-17 and pepsinogen-1 in the fasting state. Anti-H pylori IgG was found in 2,134 patients. Seven years later, 2,220 patientswho had undergone serological noninvasive screening were asked to fill out a questionnaire survey (were interviewed). We could not find any information on 627 of 2,847 patients. Next, 75 patients with multifocal atrophic gastritis who underwent gastroscopy and biopsies (the Updated Sydney System (USS)) were selected. To study gastrin-17 production, morpho-functional correlation was studies in 75 patients with multifocal atrophic gastritis.. During seven years, no reported case of gastric cancer was done among 2,220 persons who underwent serological screening and treatment. In the same population, 4.3 persons who did not receive screening during the same period, developed gastric cancer and died of it. In this study, we can say that 4.3 lives were saved out of 2,220 tested persons. The cost for screening this number of people amounted to €23,750. A comparison of the prevalence rate of the four stages of multifocal atrophic gastritis based on the data of the histopathology tests and noninvasive serologic screening in accordance with OLGA classification showed a strong correlation (the correlation coefficient is 0.812). This finding suggested that using this classification not only for histopathology tests for atrophic gastritis but also for serologic markers of antral mucosa and corpus ventriculi atrophy: gastrin-17 and pepsinogen-1.. Complex pathogenetic treatment of atrophic gastritis significantly reduced gastric cancer risk and incidence for such patients.
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Topics: Adult; Antineoplastic Combined Chemotherapy Protocols; Biomarkers; Case-Control Studies; Female; Follow-Up Studies; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Mass Screening; Pepsinogen A; Precancerous Conditions; Prognosis; Prospective Studies; Stomach Neoplasms

Helicobacter pylori (Hp) infection affects a substantial proportion of the world population and is a major risk factor of gastric cancer (GC). The caveats of common Hp-tests can be evaded by a serological biomarker test (GastroPanel®, Biohit Oyj, Helsinki), the most comprehensive Hp-test on the market. The clinical validation of Helicobacter pylori IgG ELISA of the new-generation GastroPanel® test is reported. The aim of the study is to validate the clinical performance of the Helicobacter pylori IgG ELISA test in diagnosis of biopsy-confirmed Hp-infection in gastroscopy referral patients.. A cohort of 101 patients (mean age=50.1 years) referred for gastroscopy at the outpatient Department of Gastroenterology (SM Clinic, St. Petersburg) were examined by two test versions to validate the new-generation GastroPanel®. All patients were examined by gastroscopy and biopsies, which were stained with Giemsa for specific identification of Hp in the antrum (A) and corpus (C).. Biopsy-confirmed Hp-infection was found in 64% of patients, most often confined to antrum. The overall agreement between Hp IgG ELISA and gastric biopsies in Hp-detection was 91% (95%CI=84.1-95.8%). Hp IgG ELISA diagnosed biopsy-confirmed Hp (A&C) with sensitivity (SE) of 92.3%, specificity (SP) of 88.6%, positive predictive value (PPV) of 93.8% and negative predictive value (NPV) of 86.1%, with AUC=0.904 (95%CI=0.842-0.967). In ROC analysis for Hp detection (A&C), Hp IgG ELISA shows AUC=0.978 (95%CI=0.956-1.000).. The Hp IgG ELISA test successfully concludes the clinical validation process of the new-generation GastroPanel® test, which retains the unrivalled diagnostic performance of all its four biomarkers, extensively documented for the first-generation test in different clinical settings.

Topics: Adolescent; Adult; Antibodies, Bacterial; Biopsy; Enzyme-Linked Immunosorbent Assay; Female; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Referral and Consultation; Stomach; Stomach Neoplasms; Young Adult

Epidemiological studies found a significant correlation between Helicobacter pylori infection and elevated serum pepsinogen, especially pepsinogen II (PGII), and reduced pepsinogen I (PGI)/PGII ratio. The study aimed to evaluate the association between abnormal gastric function risk and H. pylori infection assessed by H. pylori IgG assay and (14)C-urea breath test (UBT).. A total of 1555 subjects who underwent a health check were enrolled. Serum PGI, serum PGII, PGI/PGII ratio, gastrin 17 (G17), H. pylori IgG antibody titer, and UBT results were collected.. Median PGII and G17 levels were higher, but PGI/PGII ratio was lower in H. pylori-seropositive compared with seronegative participants (P<0.001, respectively). Similar effects were demonstrated by UBT. The consistency between H. pylori IgG assay, and UBT results were 86.9%, 82.29%, and 84.64% in individuals with normal gastric function, but only 73.4%, 67.98%, and 74.6% in those with abnormal gastric function. The correlation coefficients for H. pylori infection and abnormal gastric function diagnosed by PGI/PGII <7 were 0.336 (P<0.001) by H. pylori IgG assay and 0.231 (P<0.001) by UBT, diagnosed by PGII ≥ 8.25 µg/L were 0.594(P<0.001) by H. pylori IgG assay and 0.493 (P<0.001) by UBT, diagnosed by G17 >3 pmol/L was 0.469 (P<0.001) by H. pylori IgG assay and 0.394 (P<0.001) by UBT. The odds ratios (ORs) (95% confidence intervals) of abnormal gastric function were 7.477 (5.278-10.594), 19.204 (14.526-25.387), and 7.921 (6.286-9.982) comparing positive versus negative by H. pylori IgG assay and 4.084 (2.98-5.598), 9.552 (7.494-12.174), and 5.402 (4.335-6.731) comparing positive versus negative by UBT.. H. pylori infection assessments by antibody-based or bacterial component-based detection are both related with abnormal gastric function. Moreover, serum H. pylori IgG assay was stronger associated with abnormal gastric function than UBT assay.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Breath Tests; Enzyme-Linked Immunosorbent Assay; Female; Gastric Mucosa; Gastrins; Helicobacter Infections; Humans; Immunoglobulin G; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Retrospective Studies; Stomach; Urea; Young Adult

The aim of this study was to assess the gastric histopathology and serum gastrin-17 and pepsinogens profiles in patients with duodenal ulcer before and after Helicobacter pylori eradication in a population with a very high prevalence of H. pylori. At the same time we assessed the role of H. pylori density on these variables.. Eighty Caucasian patients with H. pylori-associated duodenal ulcer before treatment and 1 year after randomized eradication were studied. Among patients with unsuccessful eradication two groups were distinguished according to the data obtained after treatment: the group with negative rapid urease test and decreased bacterial density according to morphological score (partial elimination group); the group with positive rapid urease test and high bacterial density (failed eradication group).. One year after successful eradication, serum levels of gastrin-17, pepsinogen I and pepsinogen II decreased. Similar changes of serum pepsinogen I and pepsinogen II levels were observed in patients with partial elimination of H. pylori infection. In the group with successful eradication, inflammation, activity, atrophy and number of lymphoid follicles in the antral mucosa fell. In the group with partial elimination, antral mucosa activity and H. pylori score reduced. Other morphological changes were statistically non-significant.. Patients with duodenal ulcer after successful eradication have improvement of morphological and functional characteristics of gastric mucosa.

Topics: Adolescent; Adult; Anti-Bacterial Agents; Antibodies, Bacterial; Biomarkers; Down-Regulation; Drug Therapy, Combination; Duodenal Ulcer; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Proton Pump Inhibitors; Time Factors; Treatment Failure; Treatment Outcome; Urease; Young Adult

To assess the possibility of non-invasive screening of atrophic chronic gastritis for preventing further development of gastric cancer.. One hundred and seventy-eight consecutive Helicobacter pylori (H pylori)-positive dyspeptic patients after detection of serum levels of pepsinogen-1 (PG-1) and gastrin-17 (G-17) by enzyme immunoassay were proposed for endoscopy and histology. The serologic and morphologic results were compared with estimating the sensitivity, specificity and prognostic values of the tests.. There was statistically significant reverse dependence between the grade of stomach mucosal antral or corpus atrophy and the proper decreasing of serum G17 or PG1 levels. The serologic method was quite sensitive in the diagnosis of non-atrophic and severe antral and corpus gastritis. Also, it was characterized by the high positive and negative prognostic values.. Detection of serum G-17 and PG1 levels can be offered as the screening tool for atrophic gastritis. The positive serologic results require further chromoendoscopy with mucosal biopsy, for revealing probable progressing of atrophic process with development of intestinal metaplasia, dysplasia or gastric cancer.

Topics: Atrophy; Biomarkers; Biopsy; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunoenzyme Techniques; Mass Screening; Pepsinogen A; Precancerous Conditions; Sensitivity and Specificity

The aim of the study was to determine the proportion of gastric cancer patients with decreased levels of pepsinogen and gastrin-17 in plasma, with the goal of providing indirect evidence of the sensitivity of these biomarkers when applied in a cancer screening setting.. The levels of pepsinogens I and II, gastrin-17, and Helicobacter pylori immunoglobulin antibodies in plasma samples of gastric cancer patients were evaluated using the GastroPanel test system (Biohit Oyj, Helsinki, Finland). A decreased level of the pepsinogen I/II ratio was defined as less than three, while a decrease in gastrin-17 was defined as less than 1 pmol/L. Univariate analysis using non-parametric tests was used to investigate differences between normal and low concentrations of biomarkers.. In total, 481 plasma samples from patients (59.9% male) with a median age of 64 years (ranging from 27 to 88 years) were analyzed. Out of the 400 cases of gastric cancer (83.2% of the total), 182 were categorized as the intestinal type, 141 as the diffuse type, 60 as the mixed type, and 17 as indeterminate according to the Lauren classification system. The H. pylori immunoglobulin test was positive in 74.0% of the patients. Pepsinogen I/II ratio was decreased in 32.4% (36.8% of the intestinal type); gastrin-17 in 12.3% (10.1% of the antral region) of all cases.. The majority of gastric cancer patients had normal levels of pepsinogen and gastrin-17, suggesting that these biomarkers have limited application as screening tools in the Caucasian population.

Topics: Antibodies, Bacterial; Biomarkers; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Stomach Neoplasms

In Mongolia, gastric cancer morbidity and mortality are high, and more than 80 percent of cases are diagnosed at an advanced stage. This study aimed to evaluate pepsinogens (PGIs) and gastrin-17 (G-17) levels and to determine the diagnostic performances for gastric cancer and chronic atrophic gastritis among Mongolian individuals. We enrolled a total of 120 subjects, including gastric cancer (40), atrophic gastritis (40), and healthy control (40), matched by age (±2) and sex. Pepsinogen I (PGI), Pepsinogen II (PGII), G-17, and H. pylori IgG levels were measured using GastroPanel ELISA kit (Biohit, Helsinki, Finland). Also, PGI to PGII ratio (PGR) was calculated. For atrophic gastritis, when the optimal cut-off value of PGI was ≤75.07 ng/ml, the sensitivity and specificity were 75% and 50%, respectively; when the optimal cut-off value of PGR was ≤6.25, sensitivity and specificity were 85% and 44.7%, respectively. For gastric cancer, when the optimal cut-off value of PGI was ≤35.25 ng/ml, the sensitivity and specificity were 47.2% and 86.8%, respectively; when the optimal cut-off value of PGR was ≤5.27, sensitivity and specificity were 75% and 60.5%, respectively. Combinations of biomarkers with risk factors could improve diagnostic accuracy (AUC for atrophic gastritis 74.8, 95% CI 64.0-85.7, p<0.001; AUC for gastric cancer 75.5, 95% CI 64.2-86.8, p<0.001). PGI, PGR biomarkers combined with the risk of age, family history of gastric cancer, and previous gastric disease could not be an alternative test for upper endoscopy but might be a supportive method which is identifying individuals at medium- and high risk of gastric cancer and precancerous lesions who may need upper endoscopy.

Topics: Biomarkers; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Pepsinogen A; Pepsinogen C; Stomach Neoplasms

To explore the value of the Helicobacter pylori test in combination with the determination of plasma pepsinogen (PG) and gastrin 17 in screening the precancerous status of gastric cancer and gastric cancer in the healthy population, between 2019 and 2022, we enrolled a total of 402 subjects who went to the physical examination in the Center of Health Management of Ganzhou people's Hospital and additionally underwent the urea (14C) breath test and determination of PGI, PGII and G-17. Anomalies in Hp, PG or G-17 ≥ 2, or a single anomaly in PG determination would be taken as positive, and the diagnosis should be further confirmed by the gastroscopy and pathological test. According to the results, subjects would be further divided into the gastric cancer group, precancerous lesion group, precancerous disease group and control group, aiming to clarify the relationship between Hp, PG and G-17 levels and the precancerous status and development of gastric cancer and the screening value. Results showed that Hp-positive infection was found in 341 subjects (84.82%). Hp infection rate in the control group was much lower than those in the precancerous disease group, precancerous lesion group and gastric cancer group (P < 0.05). The CagA positive rates in the gastric cancer group and precancerous lesion group were significantly higher than those in the precancerous disease group and control group, while the serum level of G-17 in the gastric cancer group was much higher than those in the precancerous lesion group, precancerous disease group and control group (P < 0.05), and the PG I/II ratio in the gastric cancer patients was also lower than those in the precancerous lesion group, precancerous disease group and control group (P < 0.05). As the disease progressed, the G-17 level also increased but PG I/II ratio decreased gradually (P < 0.001). Hp test in combination with PG and G-17 shows a high value in determining the precancerous status of gastric cancer and screening for gastric cancer in healthy subjects.

Topics: Early Detection of Cancer; Helicobacter Infections; Helicobacter pylori; Humans; Pepsinogen A; Pepsinogen C; Precancerous Conditions; Stomach Neoplasms

Prompted by the increasing demand of non-invasive diagnostic tools for screening of gastric cancer (GC) risk conditions, i.e., atrophic gastritis (AG) and Helicobacter pylori (Hp) infection, the GastroPanel. Altogether, 522 patients were enrolled among the patients referred for gastroscopy at the Gastro Center, Oulu University Hospital (OUH). All patients underwent gastroscopy with biopsies classified using the Updated Sydney System (USS), and blood sampling for GP testing.. The new generation GastroPanel

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Antibodies, Bacterial; Biomarkers; Biopsy; Enzyme-Linked Immunosorbent Assay; Female; Finland; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Host-Pathogen Interactions; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Predictive Value of Tests; Referral and Consultation; Reproducibility of Results; Serologic Tests; Young Adult

Analysis of serum biomarkers for the assessment of atrophic gastritis (AG), considered as gastric precancerous lesion, is of growing interest and recommended by current guidelines. Our aim was to evaluate the diagnostic performance of a panel of biomarkers (GastroPanel®) for the detection of AG in France, a country of a low gastric cancer (GC) incidence.. In this prospective, multicenter, cross-sectional study, consecutive patients considered at increased risk of GC and undergoing upper endoscopy with gastric biopsies were included. Blood samples were collected for the analysis of GastroPanel® (association of Pepsinogens I and II, Gastrin-17, and Helicobacter pylori serology) using ELISA. The results of GastroPanel® were compared to the results of histology considered as the reference.. Between 2016 and 2019, 344 patients (148 cases with AG, 196 controls without AG) were included. Sensitivity, specificity, positive, and negative predictive values for the detection of AG by GastroPanel® were of 39.9% (95% CI 31.9; 48.2), 93.4% (95% CI 88.9; 96.4), 81.9 (95% CI 71.1; 90.0), and 67.3 (95% CI 61.4; 72.8), respectively. The sensitivity was significantly higher for the detection of severe AG [60.8% (95% CI 46.1; 74.6) P = .015] and corpus AG [61.0% (95% CI 49.2; 72.0), P = .004]. Diagnostic performances of GastroPanel® tended to be better than those of Pepsinogen I alone, but the difference did not reach statistical significance (P = .068).. Serum pepsinogen and GastroPanel® tests show promising results for the detection of AG, especially of corpus AG and severe AG, in patients at high risk of GC in France.

Topics: Adult; Aged; Antibodies, Bacterial; Biomarkers; Cross-Sectional Studies; Enzyme-Linked Immunosorbent Assay; Female; France; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Humans; Incidence; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Prospective Studies; Sensitivity and Specificity; Stomach Neoplasms

Gastrin-17 (G-17) and Helicobacter pylori (H pylori) antibody are widely used in the screening of gastric diseases, especially in gastric cancer. In this study, we aimed to evaluate the value of G-17 and H pylori antibody in gastric disease screening.. Healthy males and females (1368 and 1212, respectively) aged between 21-80 years were recruited for the study. Serum G-17 value was measured using ELISA, and H pylori antibodies were measured using Western blotting. Statistical analyses were performed using the chi-square, Mann-Whitney U, and Kruskal-Wallis H tests.. Serum G-17 level was higher in the H pylori-positive group than in the negative group. Serum G-17 level was higher in the type 1 H pylori-positive group than in the type 2 H pylori-positive group. Further, serum G-17 level was higher in females than in males and showed significant differences among different age-groups, with changes in trend proportional to the age. The positive rate of H pylori infection in all the subjects was 58.29% and did not show a significant difference between males and females. However, it showed significant differences among different age-groups, with the changing trend proportional to the age.. Analysis of serum G-17 level and H pylori antibody typing is valuable in gastric disease screening. Every laboratory should establish its own reference interval for G-17 level.

Topics: Adult; Aged; Aged, 80 and over; Antibodies, Bacterial; China; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Retrospective Studies; Stomach Diseases; Young Adult

Chronic atrophic autoimmune gastritis (CAAG) can lead to the development of gastric neuroendocrine tumors (gNETs) and can be accompanied by other autoimmune diseases. This study aimed to determine, in CAAG patients, the association of gNET development, the prevalence of autoimmune diseases other than CAAG, the association of autoimmunity, and gNET development with pepsinogen I, II, gastrin-17, and Helicobacter pylori infection analysis.. We determined the prevalence of gNETs and other autoimmune diseases and analyzed pepsinogen I and II, gastrin-17 serum levels, and H. pylori infection in all patients diagnosed with CAAG at our hospital between 2013 and 2017.. A total of 156 patients were studied and in 15.4% was observed concomitant gNET. Approximately 68.6% had at least 1 other autoimmune disease at diagnosis of CAAG. Approximately 60.9% had autoimmune thyroiditis, followed by diabetes (19.9%) and autoimmune polyendocrine syndrome (12.8%). CAAG patients with and without gNET had similar rates of comorbidity with other autoimmune diseases, but the pepsinogen I/II ratio was lower in patients with gNET (1.6 vs 4.5, P = 0.018). Receiver operating characteristic curve analyses identified a pepsinogen I/II ratio <2.3 and gastrin-17 levels >29.6 pmol/L as cutoffs distinguishing CAAG patients with gNET from those without. The combined use of these cutoff correctly identified 16 of the 18 CAAG patients with gNET (P = 0.007). H. pylori infection was observed in 28.7% of cases tested but did not associate with gNET.. This study suggests that a low pepsinogen I/II ratio and high gastrin-17 levels characterize patients with CAAG and gNET and confirms the frequent coexistence of CAAG with other autoimmune diseases.

Topics: Adolescent; Adult; Aged; Autoimmune Diseases; Biomarkers; Diagnosis, Differential; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Neuroendocrine Tumors; Pepsinogen A; Pepsinogen C; Prevalence; Retrospective Studies; ROC Curve; Stomach Neoplasms; Young Adult

Screening and timely treatment of precancerous gastric cancer diseases or of gastric cancer in the early stages has important significance in reducing the incidence and mortality of gastric cancer. Gastroscopy and histopathological biopsy are still the gold standards for the diagnosis of gastric diseases. But the application of astroscopy for the screening and diagnosis of gastric diseases is limited. In recent years, serum pepsinogen (PG), gastrin, and Helicobacter pylori (H. pylori) IgG antibodies have become indicators for "serological biopsy" of the gastric mucosa.. From January 2016 to January 2018, a total of 2,394 patients with digestive tract symptoms underwent gastroscopy. According to the endoscopic examination and pathological diagnosis, there were four case groups: 1,376 cases of chronic non-atrophic gastritis, 708 cases of chronic atrophic gastritis, 265 cases of gastric ulcer, and 45 cases of gastric cancer. Serological gastric biopsies were performed and analyzed.. The serum levels of PGI in the chronic atrophic gastritis group was significantly lower than that in the chronic non-atrophic gastritis group, gastric ulcer group, and gastric cancer group (p < 0.05). The serum levels of PGII and G-17 in the gastric cancer group were significantly higher than those in the chronic non-atrophic Gastritis group, chronic atrophic gastritis group, and gastric ulcer group (p < 0.05). The PGR in the gastric cancer group was significantly lower than that in the chronic non-atrophic gastritis group, chronic atrophic Gastritis group, and gastric ulcer group (p < 0.05). The H. pylori positive rates in the chronic atrophic gastritis group and gastric cancer group were higher than those in the chronic non-atrophic gastritis group and gastric ulcer Group (p < 0.05).. Serological gastric biopsy is closely correlated to gastric mucosal disease and can be used as a Screening tool in gastric disease.

Topics: Adult; Aged; Aged, 80 and over; Antibodies, Bacterial; Biomarkers; Biopsy; Female; Gastric Mucosa; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Sensitivity and Specificity; Stomach Neoplasms; Young Adult

To develop a gastric cancer (GC) risk prediction rule as an initial prescreening tool to identify individuals with a high risk prior to gastroscopy.. This was a nationwide multicentre cross-sectional study. Individuals aged 40-80 years who went to hospitals for a GC screening gastroscopy were recruited. Serum pepsinogen (PG) I, PG II, gastrin-17 (G-17) and anti-. The novel GC risk prediction rule comprised seven variables (age, sex, PG I/II ratio, G-17 level,. The developed and validated prediction rule showed good performance on identifying individuals at a higher risk in a Chinese high-risk population. Future studies are needed to validate its efficacy in a larger population.

Topics: Adult; Aged; Aged, 80 and over; Antibodies, Bacterial; Biomarkers, Tumor; Diet; Early Detection of Cancer; Female; Gastrins; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Mass Screening; Middle Aged; Pepsinogen A; Pepsinogen C; Predictive Value of Tests; Random Allocation; Reproducibility of Results; Risk Factors; Secondary Prevention; Stomach Neoplasms

Whether gastric hyperchlorhydria and Helicobacter pylori infection contribute to aspirin-induced gastroduodenal injury still lacks evidence. Because serum pepsinogens (PGs) and gastrin-17 (G17) can reflect gastric acid secretion, this study intended to elucidate whether serum PGs, serum G17, and H. pylori infection are associated with aspirin-induced gastrointestinal injury.. A total of 60 patients taking low-dose aspirin for more than 1 month were enrolled in this study. Serum PG I, PG II, and G17 were determined using ELISA. A 14C-urea breath test was used for the detection of an H. pylori infection. The modified Lanza score was used to evaluate the degree of gastroduodenal injury under endoscopy. The median serum PG I level was significantly higher in the intensive gastroduodenal injury (IGI) group compared to that in the mild gastroduodenal injury group (155.0 vs. 116.6 ng/mL, p = 0.006). The H. pylori infection rate was significantly higher in the IGI group (73 vs. 40%, p = 0.037). Receiver operator characteristic curves analysis revealed that the cutoff value of PG I was 123 ng/mL, with 80% sensitivity and 61.4% specificity. H. pylori infection combined with PG I at >123 ng/mL had an OR (95% CI) of 15.8 (2.4 ± 104.5) for the prediction of aspirin-induced gastroduodenal injury. Key Messages: Serum PG I and H. pylori infection could be used to identify potential high-risk aspirin-induced gastroduodenal injury patients.

Topics: Aged; Area Under Curve; Aspirin; Duodenum; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Multivariate Analysis; Pepsinogen A; Risk Factors; ROC Curve; Stomach

Studies have suggested that Helicobacter pylori (Hp) infection is associated with atherosclerotic process, while the relationship between pepsinogens, gastrin and atherosclerosis is unknown.. The aim of the study was to observe association of Hp infection on atherosclerotic parameters and blood pressure, and explore the relationship between atherosclerotic parameters, blood pressure and gastric biomarkers in a healthy population.. 395 subjects were chosen and received physical examinations, carotid artery ultrasound, peripheral atherosclerosis measurement, and testing of serum pepsinogen (PG) I and II, Hp antibody, and gastrin-17 (G-17) levels. Analyses were conducted by Student's t-test, ANOVA, Pearson correlation, multiple linear regression and binary logistic regression.. In Hp-infected subjects, right carotid intima media thickness (R-CIMT) were higher (P = 0.027) and left ankle brachial index were higher in 45-64 years compared to 35-44 years group (P = 0.039, P = 0.016). Hp-IgG, PGI and G-17 respectively positively correlated with CIMT, pulse wave velocity and systolic blood pressure (P = 0.044, P = 0.013, P = 0.021). The unadjusted OR in subjects with elevated CIMT for quartile IV of PGI was 3.542 (95% CI, 1.491-8.411), the adjusted OR was 2.916 (95% CI, 1.035-8.216). The unadjusted OR in subjects with elevated CIMT for quartile III of G-17 was 4.351 (95% CI, 1.670-11.336) and for quartile IV was 3.108 (95% CI, 1.149-8.406), the adjusted OR for quartile III was 4.962 (95% CI, 1.515-16.258).. Hp infection, higher levels of PGI and G-17 may contribute to atherosclerotic process by influencing atherosclerotic parameters and blood pressure in a healthy population, the influence on CIMT was most significant.

Topics: Adult; Age Factors; Aged; Aged, 80 and over; Atherosclerosis; Biomarkers; Carotid Intima-Media Thickness; China; Cross-Sectional Studies; Female; Gastrins; Healthy Volunteers; Helicobacter Infections; Helicobacter pylori; Humans; Logistic Models; Male; Middle Aged; Pepsinogens; Pulse Wave Analysis; Risk Factors

To assess characteristics of oxyntic gastric atrophy (OGA) in autoimmune gastritis (AIG) compared with OGA as a consequence of Helicobacter pylori infection.. Patients undergoing oesophagogastroduodenoscopy from July 2011 to October 2014 were prospectively included (N=452). Gastric biopsies were obtained for histology and H. pylori testing. Serum gastrin-17 (G17), pepsinogen (PG) I, PGII and antibodies against H. pylori and cytotoxin-associated gene A protein were determined in all patients. Antibodies against parietal cells and intrinsic factor were determined in patients with advanced (moderate to severe) OGA. Areas under the receiver operating characteristic curves (AUCs) were calculated for serum biomarkers and compared with histology.. Overall, 34 patients (8.9%) had advanced OGA by histology (22 women, age 61±15 years). Current or past H. pylori infection and AIG were present in 14/34 and 22/34 patients, respectively. H. pylori-negative AIG patients (N=18) were more likely to have another autoimmune disease (OR 6.3; 95% CI 1.3 to 29.8), severe corpus atrophy (OR 10.1; 95% CI 1.9 to 54.1) and corpus intestinal metaplasia (OR 26.9; 95% CI 5.3 to 136.5) compared with H. pylori-positive patients with advanced OGA. Antrum atrophy was present in 39% of H. pylori-negative AIG patients. The diagnostic performance of G17, PG I and PGI/II was excellent for AIG patients (AUC=0.83, 0.95 and 0.97, respectively), but limited for H. pylori-positive patients with advanced OGA (AUC=0.62, 0.75 and 0.67, respectively).. H. pylori-negative AIG has a distinct clinical, morphological and serological phenotype compared with advanced OGA in H. pylori gastritis.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Atrophy; Autoimmune Diseases; Female; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Humans; Male; Middle Aged; Pepsinogen A; Prospective Studies; Young Adult

Effectively managing precancerous lesions is crucial to reducing the gastric cancer (GC) burden. We evaluated associations of temporal changes in multiple serological markers (pepsinogen I [PGI], PGII, PGI/II ratio, gastrin-17 and anti-Helicobacter pylori IgG) with risk for progression of gastric precancerous lesions. From 1997 to 2011, repeated esophagogastroduodenoscopies with gastric mucosal biopsies and blood sample collections were conducted on 2,039 participants (5,070 person-visits) in the Zhuanghe Gastric Diseases Screening Program, Liaoning, China. Serum biomarkers were measured using ELISA, and gastric biopsies were evaluated using standardized histologic criteria. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using generalized estimating equations for correlated binary outcomes. The ORs for progression of gastric conditions comparing those whose serum PGI, PGII, and anti-H. pylori IgG levels increased ≥ 50% relative to those whose decreased ≥ 50% were, respectively 1.67 (CI, 1.22-2.28), 1.80 (CI, 1.40-2.33) and 1.93 (CI, 1.48-2.52). The OR for those whose PGI/II ratio decreased ≥ 50% relative to those whose increased ≥ 50% was 1.40 (CI, 1.08-1.81), and for those whose PGII and anti-H. pylori IgG levels both increased ≥ 50% relative to those whose levels both decreased ≥ 50% the OR was 3.18 (CI, 2.05-4.93). Changes in gastrin-17 were not statistically significantly associated with progression. These findings suggest that temporal changes in serum PGI, PGII, PGI/II ratio, and anti-H. pylori IgG levels (especially PGII and anti-H. pylori IgG combined) may be useful for assessing and managing risk for progression of gastric precancerous lesions.

Topics: Adult; Aged; Biomarkers, Tumor; Disease Progression; Enzyme-Linked Immunosorbent Assay; Female; Follow-Up Studies; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Longitudinal Studies; Male; Middle Aged; Neoplasm Staging; Pepsinogen A; Pepsinogen C; Precancerous Conditions; Prognosis; Stomach Neoplasms

Secretion of pepsinogen I (PgI), pepsinogen II (PgII), fasting gastrin-17 (fG-17) and stimulated gastrin-17 (sG-17) changes after Helicobacter pylori eradication. Few data are available on the long-term dynamics of gastric biomarkers after H. pylori eradication.The aim of this study was to investigate the dynamics of gastric biomarkers in H. pylori-positive patients after eradication over a 3-year period and to compare the levels with initially H. pylori-negative patients.. Blood samples for the detection of gastric biomarkers were obtained from dyspeptic patients coming for upper gastrointestinal endoscopy. In H. pylori-positive patients, after eradication therapy, three follow-up blood samples were drawn after 12, 24 and 36 months; in H. pylori-negative patients, two samples were taken - at 12 and after 30 months. Median values of biomarkers in follow-up samples were compared with the baseline sample.. The final sample included 110 patients (median age 67 years, M/F ratio 27/83). In patients after H. pylori eradication (n=83) PgI, PgII, fG-17 and sG-17 had decreased significantly during a 36-month period, whereas the PgI/PgII ratio had increased significantly from 5.59 to 11.64.. In H. pylori-positive dyspeptic patients, after eradication therapy, a decrease in PgI, PgII, fG-17 and sG-17 was observed after 36 months whereas an increase in the PgI/II ratio suggested an improvement in gastric atrophy. The median levels of gastric biomarkers in patients after H. pylori eradication therapy may become similar to biomarker levels among initially H. pylori-negative individuals.

Topics: Aged; Aged, 80 and over; Biomarkers; Dyspepsia; Endoscopy, Gastrointestinal; Fasting; Female; Follow-Up Studies; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Time Factors

Toll-like receptor 4 is a part of the innate immune system and recognizes Helicobacter pylori lipopolysaccharide. The goal of this study was to analyze the role of Toll-like receptor 4 polymorphisms +896 (rs4986790) and +1196 (rs4986791) in the pathogenesis of Helicobacter pylori related gastroduodenal diseases in relation to gastric secretion and inflammation. Toll-like receptor 4 polymorphisms, serum gastrin-17 and pepsinogen I and II concentrations were determined, and gastroscopies with histopathological analyses were performed to 216 dyspeptic patients. As genotype controls, 179 controls and 61 gastric cancer patients were studied. In our study, the Toll-like receptor 4 +896 and +1196 polymorphisms were in total linkage disequilibrium. The homozygous wild types displayed higher gastrin-17 serum concentrations than the mutants (p = 0.001) and this effect was independent of Helicobacter pylori. The homozygous wild types also displayed an increased risk for peptic ulcers (OR: 4.390). Toll-like receptor 4 genotypes did not show any association with Helicobacter pylori positivity or the features of gastric inflammation. Toll-like receptor 4 expression was seen in gastrin and somatostatin expressing cells of antral mucosa by immunohistochemistry. Our results suggest a role for Toll-like receptor 4 in gastric acid regulation and that the Toll-like receptor 4 +896 and +1196 wild type homozygozity increases peptic ulcer risk via gastrin secretion.

Topics: Adult; Aged; Aged, 80 and over; Female; Gastrins; Gastritis; Gene Frequency; Genetic Predisposition to Disease; Genotype; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Peptic Ulcer; Polymorphism, Single Nucleotide; Risk Factors; Stomach Neoplasms; Toll-Like Receptor 4; Young Adult

Atrophic gastritis (AG), first step in the cascade leading to gastric adenocarcinoma, is related to Helicobacter pylori (H. pylori) infection. Currently, the gold standard for the diagnosis of AG is esophagogastroduodenoscopy (EGD) with histological examination of the biopsy specimens. However, since the latter are taken in random order and the distribution of AG is often patchy, histology is only representative of mucosal status. Considering this limitation, a test named GastroPanel®, that measures the blood concentrations of pepsinogen I and II, gastrin-17 and H. pylori antibodies, has been developed as a potential non-invasive biopsy. Aim of this study has been to assess the accuracy of GastroPanel® in patients with AG.. Forty-seven dyspeptic patients (24 males, mean age 52.2±9.3 years), in follow-up for antral or diffuse AG, were enrolled. All underwent at least two EGDs with random biopsies and blood collection for GastroPanel® parameters examination.. Of the 47 patients, 16 (34.1%) had histological diagnosis of antral and 31 (65.9%) multifocal AG; 17 (36.2%) patients had mild and 30 (63.8%) had moderate-severe AG. H. pylori was detected in 39 (82.9%) and intestinal metaplasia was found in all patients. GastroPanel® showed 82.9% sensitivity for the diagnosis of AG and 53.8% for the diagnosis of H. pylori infection. The prediction of advanced atrophy was not sufficiently accurate, neither in patients with antral nor in those with multifocal AG.. GastroPanel® can be useful for detecting patients with AG. However, it does not reflect the severity of atrophy.

Topics: Adult; Antibodies, Bacterial; Biomarkers; Biopsy; Dyspepsia; Endoscopy, Digestive System; Female; Follow-Up Studies; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Predictive Value of Tests; Sensitivity and Specificity; Severity of Illness Index

It 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.. To determine the accuracy of GastroPanel for the diagnosis of CAG.. This 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.. Ninety-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.. GastroPanel is not accurate enough for the diagnosis of CAG; thus, its systematic use in clinical practice cannot be recommended.

Topics: Adult; Algorithms; Antibodies, Bacterial; Biomarkers; Biopsy; Chronic Disease; Double-Blind Method; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Predictive Value of Tests; Prospective Studies; Pyloric Antrum; Stomach

Pepsinogen levels in plasma are increased by inflammation in the gastric mucosa, including inflammation resulting from Helicobacter pylori infection. A decrease in pepsinogen II level has been suggested as a reliable marker to confirm the successful eradication of infection. The aim of our study was to evaluate the potential role of pepsinogens I and II, gastrin-17 and H. pylori antibodies in confirming successful eradication.. Altogether 42 patients (25 women, 17 men), mean age 45 years (range 23-74), were enrolled. Pepsinogens I and II, gastrin-17 and H. pylori IgG antibodies were measured in plasma samples using an ELISA test (Biohit, Oyj., Finland) before the eradication and 4 weeks after completing the treatment. The success of eradication was determined by a urea breath test.. Eradication was successful in 31 patients (74%) and unsuccessful in 11 patients (26%). Pepsinogen II decreased significantly in both the successful (P=0.029) and unsuccessful (P=0.042) eradication groups. Pepsinogen I decreased significantly in the successful (P=0.025) but not the unsuccessful (P=0.29) eradication group. The pepsinogen I/II ratio increased in the successful eradication group (P=0.0018) but not in the group in which treatment failed (P=0.12). There were no differences in gastrin-17 or H. pylori antibody values.. A decrease in pepsinogen II levels cannot be used as a reliable marker for the successful eradication of H. pylori 4 weeks after the completion of treatment. The increase in pepsinogen I/II ratio reflects differences in pepsinogen production following the eradication irrespective of improvement in atrophy.

Topics: Adult; Aged; Antibodies, Bacterial; Biomarkers; Female; Gastric Mucosa; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Treatment Outcome; Young Adult

Fasting serum gastrin-17 (FsG17) is considered as a noninvasive biomarker reflecting the structure and functional status of gastric mucosa, but its clinical utility remains unclear. This study aimed to evaluate FsG17 comprehensively: establish the ranges and cut-off points of FsG17 levels in different gastric diseases, identify their influencing factors, and investigate the accuracy of FsG17 for identifying diseased stomach.. The study included 4064 participants from Northern China between 2008 and 2013. FsG17 and serum Helicobacter pylori IgG antibody levels were measured by enzyme-linked immunosorbent assay. Diagnostic accuracy was assessed by receiver operator characteristic curves. Multivariate logistic regression analysis was performed to determine the best predictors of gastric histopathological conditions.. Median FsG17 levels in healthy, non-atrophic, atrophic, and cancerous stomachs were 1.8, 4.0, 3.8, and 6.1 pmol/l, respectively. Age, smoking status, alcohol consumption, H. pylori infection, and predominant lesion site were factors that affected FsG17 levels. The optimal cut-off values for FsG17 were 3.0 pmol/l (sensitivity of 59.3% and specificity of 67.3%) for discriminating between healthy stomach and diseased stomach and 10.7 pmol/l (sensitivity of 37% and specificity of 83.7%) for discriminating between cancerous stomach and cancer-free stomach; the screening accuracy was higher (sensitivity of 50.0% and specificity of 83.0%) for gastric cancer in the corpus. Multivariate analysis showed that FsG17, gender, age, and H. pylori infection were independent predictors of cancerous stomach.. With the progression from health stomach to malignancy, FsG17 levels significantly increased and were influenced by other factors. FsG17 combined with age, gender, and H. pylori infection could distinguish between cancerous stomach and cancer-free stomach. The results will enhance our understanding of the potential clinical utility of FsG17.

Topics: Age Factors; Alcohol Drinking; Area Under Curve; Biomarkers; China; Fasting; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Male; Middle Aged; Predictive Value of Tests; ROC Curve; Smoking; Stomach Neoplasms

Gastric cancer (GC) is the second cause of cancer related death in the world. It may develop by progression from its precancerous condition, called gastric atrophy (GA) due to gastritis. The aim of this study was to evaluate the accuracy of serum levels of pepsinogens (Pg) and gastrin-17 (G17) as non-invasive methods to discriminate GA or GC (GA/GC) patients.. Subjects referred to gastrointestinal clinics of Golestan province of Iran during 2010 and 2011 were invited to participate. Serum levels of PgI, PgII and G17 were measured using a GastroPanel kit. Based on the pathological examination of endoscopic biopsy samples, subjects were classified into four groups: normal, non-atrophic gastritis, GA, and GC. Receiver operating curve (ROC) analysis was used to determine cut-off values. Indices of validity were calculated for serum markers.. Study groups were normal individuals (n=74), non-atrophic gastritis (n=90), GA (n=31) and GC patients (n=30). The best cut-off points for PgI, PgI/II ratio, G17 and HP were 80 μg/L, 10, 6 pmol/L, and 20 EIU, respectively. PgI could differentiate GA/GC with high accuracy (AUC=0.83; 95%CI: 0.76-0.89). The accuracy of a combination of PgI and PgI/II ratio for detecting GA/GC was also relatively high (AUC=0.78; 95%CI: 0.70-0.86).. Our findings suggested PgI alone as well as a combination of PgI and PgI/II ratio are valid markers to differentiate GA/GC. Therefore, Pgs may be considered in conducting GC screening programs in high-risk areas.

Topics: Adult; Antibodies, Bacterial; Case-Control Studies; Cross-Sectional Studies; Early Detection of Cancer; Female; Gastrins; Gastritis; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Iran; Male; Middle Aged; Pepsinogen A; Pepsinogen C; ROC Curve; Sensitivity and Specificity; Stomach Neoplasms

In Fujian Province, China, gastric cancer is one of the leading causes of mortality among all malignant tumors. Nanjing county and Minqing county are located in inland Fujian and have similar general demographics. However, the adjusted mortality rate of gastric cancer in Minqing was found to be much higher than that in Nanjing. We sought to explore factors associated with this increased risk of gastric cancer between the two counties.. We recruited 231 and 224 residents from Nanjing and Minqing, respectively, and analyzed differences between their dietary habits, Helicobacter pylori infection rates, and concentrations of serum pepsinogen I, pepsinogen II, gastrin-17, and ratio of pepsinogen I:II.. Subjects in Minqing had more first-degree relatives who had been diagnosed with upper gastrointestinal tumor, more unhealthy dietary habits, a higher Helicobacter pylori positive rate, and greater proportion of abnormal serum gastrin-17 than those in Nanjing did.. The factors that differed between these two counties might indicate that residents in Minqing have a higher risk for developing gastric cancer than those in Nanjing do.

Topics: Adult; Aged; China; Feeding Behavior; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Risk Factors; Stomach Neoplasms

The aim of this study was to investigate the value of serum gastric markers to differentiate between patients with precancerous lesions and nonatrophic chronic gastritis.. Serum samples of 128 patients with dyspepsia who were candidates for endoscopic examination were tested for pepsinogen (PG I and PG II), PG I/II ratio, gastrin 17(G-17), anti-Helicobacter pylori (anti-H pylori ) and anti- CagA antibodies. Two sample t-tests, chi-square tests and Pearson's correlation analyses were used for analysis using SPSS (version 20).. PGI, PG I/II ratio values were decreased significantly in the precancerous lesion group (0.05, 0.001 respectively). The frequency of H pylori infection was significantly (p=0.03) different between the two groups ofthe study.. We suggest PGI and the PG I/II ratio as valuable markers for screening of premalignant gastric lesions.

Topics: Aged; Antibodies, Bacterial; Antigens, Bacterial; Bacterial Proteins; Biomarkers; Chronic Disease; Cross-Sectional Studies; Dyspepsia; Female; Follow-Up Studies; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Iran; Male; Pepsinogen A; Pepsinogen C; Precancerous Conditions; Prognosis; Stomach Neoplasms

The article is devoted to the problem of diagnostics of atrophic gastritis. The main principles of morphological diagnostics are presented. The endoscopic findings are discussed. The authors had used the mathematical regression model to reveal groups of patients with some specific signs of atrophic gastritis, such as endoscopic sings, morphological and clinical signs. This model can be used to put a diagnosis and to look after the patients with metaplasia, dysplasia and early cancer.

Topics: Biopsy; Decision Trees; Diagnosis, Differential; Endoscopy, Gastrointestinal; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Metaplasia; Models, Biological; Pepsinogens; Prognosis

Helicobacter pylori-infection associated gastritis is known to be a significant risk factor of gastric cancer. Serum levels of Gastrin-17 and Pepsinogen1which are respectively biomarkers of gastric antral and corpus mucosal activity are well known parameters of atrophic gastritis.. To determine the prevalence of Helicobacter pylori and atrophic gastritis amongst dyspeptic patients and to compare the production of PGI and G-17 in the various atrophic stages.. A total of 139 dyspeptic patients aged 46.68±15.50 years [females 106 aged47.23±15.51years, males 33 aged 44.48±14.62] were included during the one year period, March 2008-april 2009 at the district hospital Tombel. The degree of atrophy was determined by the levels of serum pepsinogen1, and gastrin-17 and the presence of Helicobacter pylori antibodies detected by an enzyme immunoassay.. The prevalence of Helicobacter pylori was 79.82% and that for atrophic gastritis was 6.6%. A decrease in mean serum levels of gastin-17 along with increasing antral atrophy was observed; the mean serum levels of pepsinogen1 were reduced during progression of corpus atrophy.. A weak reverse correlation(r =-0.036) was found between Gastrin-17 and Helicobacter pylori antibodies.

Topics: Adult; Aged; Aged, 80 and over; Algorithms; Antibodies, Bacterial; Cameroon; Cross-Sectional Studies; Dyspepsia; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoenzyme Techniques; Male; Middle Aged; Pepsinogen A; Prevalence; Risk Factors; Socioeconomic Factors; Surveys and Questionnaires; Young Adult

Health authorities of Kazakhstan are seeking for effective measures to interrupt the untoward trend, projected to increase the current number of gastric cancer (GC) cases (n=3,316) by 50% until the year 2030.. Use of a non-invasive blood test with four stomach-specific biomarkers [Pepsinogen-I (PG-I) and -II (PG-II), amidated gastrin-17 (G-17), and Helicobacter pylori (HP) IgG antibodies], to assess for the prevalence of stomach conditions: Helicobacter pylori (HP) infection and atrophic gastritis (AG), both known to increase GC risk of in Kazakhstan.. A cohort of 835 (symptomatic and asymptomatic) cases (473 women and 362 men)(median age 46.8 years; range 13.6-74.8) was examined with a panel of biomarkers. Results were assigned in five categories: 1) Healthy stomach, 2) HP infection, 3) atrophic gastritis (AG) of the antrum, 4) AG of the corpus, and 5) AG of both antrum and corpus (pangastritis).. The distribution in these five categories was identical in both sexes (p=0.259). Healthy stomach was detected only in 196 (23.5%) subjects, whereas the vast majority, 62.3% (n=519) had HP infection (with no AG). In 118 (14.1%) subjects, results were consistent with AG; in antrum (n=72), corpus (n=42) or pangastritis (n=4). Prevalence of AG increased with patient's age in both sexes. There was no age-related pattern in biomarker levels, and only slight differences between the genders.. While capable of detecting the subjects at risk for GC (HP or AG), GP seems to be a cost-effective means to intervene the current ominous trend in GC incidence in Kazakhstan.

Topics: Adolescent; Adult; Aged; Antibodies, Bacterial; Biomarkers; Dyspepsia; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Kazakhstan; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Phenotype; Prevalence; Sex Distribution; Young Adult

In a prospective study the risk of subsequent gastric cancer (GC) was assessed in persons aged 45-69 over 5 years after the initial testing with a set of serological tests (pepsinogen I, pepsinogen II, gastrin-17, antibodies to Helicobacter pylori). The presence of gastric atrophy markers was a significant predictor of GC in the forthcoming years. Non-invasive techniques may be used in the formation of high-risk groups, followed by GC active surveillance.

Topics: Aged; Antibodies, Bacterial; Biomarkers; Cohort Studies; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Pepsinogens; Retrospective Studies; Serologic Tests; Stomach Neoplasms

Non-invasive tools for gastric cancer screening and diagnosis are lacking. Serological testing with the detection of pepsinogen 1 (PG1), pepsinogen 2 (PG2) and gastrin 17 (G17) offers the possibility to detect preneoplastic gastric mucosal conditions. Aim of this study was to assess the performance of these serological tests in the presence of gastric neoplasia.. Histological and serological samples of 118 patients with gastric cancer have been assessed for tumor specific characteristics (Laurén type, localisation), degree of mucosal abnormalities (intestinal metaplasia, atrophy) and serological parameters (PG1, PG2, PG1/2-ratio, G17, H. pylori IgG, CagA status). Association of the general factors to the different serological values have been statistically analyzed.. Patients with intestinal type gastric cancer had lower PG1 levels and a lower PG1/2-ratio compared to those with diffuse type cancer (p = 0.003). The serum levels of PG2 itself and G17 were not significantly altered. H. pylori infection in general had no influence on the levels of PG1, PG2 and G17 in the serum of gastric cancer patients. There was a trend towards lower PG1 levels in case of positive CagA-status (p = 0.058). The degree of both intestinal metaplasia and atrophy correlated inversely with serum levels for PG1 and the PG1/2-ratio (p < 0.01). Laurén-specific analysis revealed that this is only true for intestinal type tumors. Univariate ANOVA revealed atrophy and CagA-status as the only independent factors for low PG1 and a low PG1/2-ratio.. Glandular atrophy and a positive CagA status are determinant factors for decreased pepsinogen 1 levels in the serum of patients with gastric cancer. The serological assessment of gastric atrophy by analysis of serum pepsinogen is only adequate for patients with intestinal type cancer.

Topics: Adenocarcinoma; Aged; Antibodies, Bacterial; Antigens, Bacterial; Atrophy; Bacterial Proteins; Biomarkers, Tumor; Female; Gastric Mucosa; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Precancerous Conditions; Retrospective Studies; Stomach Neoplasms

Gastric cancer is one of the most common malignant tumors causing death in Fujian Province, China. However, the mortality of gastric cancer is greatly varied in different areas in Fujian; for example, the mortality in Changle City is 7.4 times higher than that in Fuan City. In this study, we compared the differences in serological parameters, pepsinogen (PG) I, PG II, gastrin-17 (G-17), and Helicobacter pylori (H. pylori) antibody, between the two cities. It has been reported that low serum PG I is correlated with atrophic gastritis, a high-risk condition for developing gastric cancer, while high serum G-17 has been used for serological detection of atrophic corpus gastritis. We recruited 224 healthy subjects in Changle and 229 healthy subjects in Fuan, matched in age and sex. The serum levels of PG II and G-17 were significantly higher in Changle than those in Fuan. Importantly, the frequency of the subjects with low serum PG I (< 25 μg/L) was significantly higher in Changle than in Fuan, although the serum PG I levels were similar between the two cities. Moreover, the percentage of the subjects with high serum G-17 (≥ 2 pmol/L) and the positive rate of serum IgG antibody against H. pylori were significantly higher in Changle than those in Fuan. The detected differences in these serological parameters are consistent with the notion that the prevalence of atrophic gastritis may be higher in Changle than in Fuan, which results in a higher risk condition for developing gastric cancer in Changle.

Topics: Adult; Aged; Antibodies, Bacterial; China; Cities; Female; Gastrins; Geography; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Pepsinogens; Residence Characteristics; Stomach Neoplasms

The relationship between gastroesophageal reflux disease (GERD) and Helicobacter pylori is controversial. We evaluated endoscopic, 24-h gastric and esophageal acid profile among patients with GERD in relation to H. pylori, as the latter might alter gastric acid secretion.. Patients with GERD (n = 123), who were not on acid-suppressive drugs, and had not received anti-H. pylori therapy, underwent gastroduodenoscopy and tests for H. pylori detection. Esophageal manometry, 24-h pH metry, serum pepsinogen-I (PG-I), PG-II and gastrin-17 ELISA were done in all these patients. Univariate and multivariate analyses were performed to assess independent predictors for erosive esophagitis (EE).. Of 123 patients (mean age 40.5 [13.1] years, 85 [69.1%] men), 59 (47.9%) had H. pylori infection. EE was more common in H. pylori non-infected than infected (49 vs. 32, p < 0.001). Among patients older than 40 years, absence of H. pylori was associated with lower esophageal pH and longer reflux (p = 0.02 and p < 0.001, respectively). PG-I/PG-II ratio was lower in H. pylori infected subjects (p < 0.001). In patients with higher LA grade of esophagitis, elevated PG-I levels and PG-I/PG-II ratio were associated with more acidic stomach (p = 0.04 and p = 0.01, respectively). Multivariate analyses showed low gastrin-17 (p = 0.016), higher age (p = 0.013), hiatus hernia (p = 0.004) and absence of H. pylori (p = 0.03) were independent predictors for risk of EE.. H. pylori infection is associated with less acidic stomach and less severe GERD. Low gastrin-17, higher age, hiatus hernia and absence of H. pylori were the best predictors for EE risk.

Topics: Adult; Age Factors; Endoscopy, Digestive System; Esophagitis, Peptic; Esophagus; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastroesophageal Reflux; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Prospective Studies; Severity of Illness Index; Sex Factors

To assess the efficiency of eradication therapy in long-term period using the main signs of functional activity of gastric mucosa (gastrin-17, pepsinogen I, pepsinogen II) and serum antibodies to H. pylori.. 113 patients with chronic gastritis were examihed using clinical, endoscopic and laboratory-based methods of investigation, including GastroPanel Biohit, Finland.. It was observed that after 12 month of successful eradication therapy the titer of IgG to H. pylori did not exceed 60 IU/l, with pepsinogen I and pepsinogen II cut-off values set under 150 microg/l and 15 microg/l respectively.. The decrease of the titer of IgG to H. pylori and concentrations of pepsinogen I and II can be used as criteria of successful eradication therapy in long-term period.

Topics: Adult; Aged; Antibodies, Bacterial; Gastric Mucosa; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Time Factors

The combined evaluation of serum pepsinogens A (PGA) and C (PGC), gastrin-17 (G17) and anti-H. pylori antibodies (anti-H. pylori)(GastroPanel) has recently been proposed as a useful aid for investigating H. pylori-associated gastric mucosal inflammation. Our aim was to evaluate whether GastroPanel can correctly classify children who need or not endoscopy (EGD).. GastroPanel was performed in 554 consecutive children subjected to EGD.. PGC and anti-H. pylori were sensitive (82.5% and 73.1%) and specific (58.1% and 84.0%) indices of H. pylori infection. Antral H. pylori colonization density, inflammation and activity grades were correlated with PGC. PGC and G17 were significantly higher in children with celiac disease (14.9+/-0.88 microg/L and 5.6+/-0.79 pmol/L) than in controls (8.5+/-0.38 microg/L and 2.4+/-0.24 pmol/L). The best cut-offs to distinguish H. pylori infected children from controls were 7.45 microg/L for PGC, 4.2 pmol/L for G17, 18 U for anti-H. pylori and 25 microg/L for PGA. With these cut-offs, GastroPanel had a NPV of 89.6% and a PPV of 66.8%.. A negative GastroPanel result in children with upper abdominal non alarm symptoms, should allow the paediatrician to reasonably rule out the presence of major gastro-duodenal diseases and therefore avoid EGD.

Topics: Adolescent; Antibodies, Bacterial; Celiac Disease; Child; Child, Preschool; Endoscopy, Gastrointestinal; Female; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Diseases; Helicobacter Infections; Helicobacter pylori; Humans; Infant; Logistic Models; Male; Pepsinogen A; Pepsinogen C; Sensitivity and Specificity

To study the value of serum biomarker tests to differentiate between patients with healthy or diseased stomach mucosa: i.e. those with Helicobacter pylori (H pylori) gastritis or atrophic gastritis, who have a high risk of gastric cancer or peptic ulcer diseases.. Among 162 Japanese outpatients, pepsinogen I (Pg I) and II (Pg II) were measured using a conventional Japanese technique, and the European GastroPanel examination (Pg I and Pg II, gastrin-17 and H pylori antibodies). Gastroscopy with gastric biopsies was performed to classify the patients into those with healthy stomach mucosa, H pylori non-atrophic gastritis or atrophic gastritis.. Pg I and Pg II assays with the GastroPanel and the Japanese method showed a highly significant correlation. For methodological reasons, however, serum Pg I, but not Pg II, was twice as high with the GastroPanel test as with the Japanese test. The biomarker assays revealed that 5% of subjects had advanced atrophic corpus gastritis which was also verified by endoscopic biopsies. GastroPanel examination revealed an additional seven patients who had either advanced atrophic gastritis limited to the antrum or antrum-predominant H pylori gastritis. When compared to the endoscopic biopsy findings, the GastroPanel examination classified the patients into groups with "healthy" or "diseased" stomach mucosa with 94% accuracy, 95% sensitivity and 93% specificity.. Serum biomarker tests can be used to differentiate between subjects with healthy and diseased gastric mucosa with high accuracy.

Topics: Adult; Aged; Biopsy; Diagnosis, Differential; Gastrins; Gastritis; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Japan; Middle Aged; Outpatients; Pepsinogen A; Pepsinogen C; Peptic Ulcer; Prevalence; Reference Values; Risk Factors; Stomach; Stomach Neoplasms; Young Adult

Topics: Gastrins; Helicobacter Infections; Helicobacter pylori; Humans

Gastrin and pepsinogens reflect the functional state of the gastric mucosa.. To evaluate whether serum gastrin and pepsinogens correlate with the different grades of severity of gastro-oesophageal reflux disease (GERD).. In all, 388 patients with heartburn not taking any form of acid suppressive therapy were matched-controlled for age and gender and sub-classified into four groups: group 1 non-erosive reflux disease (NERD); group 2, erosive reflux disease (ERD) Los Angeles (LA) A and B, group 3, ERD LA C and D; group 4 Barrett's oesophagus (BO). Fasting serum was analysed for gastrin 17, pepsinogen I, pepsinogen II und Helicobacter pylori using specific EIA tests (GastroPanel; Biohit, Plc).. Kruskal-Wallis test and analysis of variance.. There was a significant difference among the four groups with respect for pepsinogen I, but not for pepsinogen II, the pepsinogen I pepsinogen II ratio, H. pylori serology and gastrin levels. Pepsinogen I was the lowest in NERD and the highest in BO (median 91.6, mean +/- standard deviation 106.2 +/- 51.6 vs. median 114.7, mean +/- standard deviation 130.4 +/- 70.6; P = 0.046). Pepsinogen I levels were higher in H. pylori positive subjects. After adjusting for H. pylori status, the differences in pepsinogen I across patient groups were no longer statistically significant (P = 0.298).. Serum gastrin and pepsinogen I and II do not correlate with the different grades of severity of GERD. The non-invasive GastroPanel is not useful for the differentiation of the various forms of GERD.

Topics: Antibodies, Bacterial; Biomarkers; Case-Control Studies; Endoscopy, Gastrointestinal; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastroesophageal Reflux; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogens; Prospective Studies

Cancer of stomach is currently regarded as the final result of a staged multifactor process during which the microenvironment affects cells and causes their changes. One of the main triggering factors is Hp infection. Adenocarcinoma of stomach develops via stages of gastritis, precancerous changes, and cancer. The possibility to prevent cancer ensues from the potential irreversibility of premalignant processes in gastric mucosa, in the first place its atrophy; hence, the importance of its early diagnosis. The state of the endoscopic service in this country is inadequate for mass screening of patients with symptoms of dyspepsia. "GastroPanel", a new serological test for the diagnosis of gastric pathology provides information about histological and functional characteristics of gastric mucosa in the antral and fundal regions of the stomach. The method determines serum gastrin-17, pepsinogen-1, and IgG expressed in response to Hp infection. Our results demonstrate high diagnostic efficiency of "GastroPanel" as a screening technique for atrophic gastritis and assessment of stomach cancer risk.

Topics: Adolescent; Adult; Aged; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Mass Screening; Middle Aged; Neoplasm Staging; Pepsinogen A; Peptide Fragments; Stomach Neoplasms; Young Adult

GastroPanel (Biohit, Helsinki, Finland) is a serum test kit that measures Helicobacter pylori antibodies (HPABs) and pepsinogens I and II and gastrin 17, which reflect the degree of atrophic gastritis. We assessed whether GastroPanel can replace endoscopic biopsies in the diagnostics of H. pylori in children and whether the H. pylori-infected children show markers for atrophic gastritis. Eighty children (median age, 6.8 years; range, 0.6-18.7 years) underwent gastroscopy for H. pylori-related abdominal complaints (n = 40), surveillance after surgery for gastrointestinal tract malformations (n = 20), gastroesophageal reflux (GER) (n = 10), and miscellaneous diseases (n = 10). Gastric biopsies and a serum sample were obtained from all 80 children. HPAB levels of 38 and 15 IU were tested as cutoff values for H. pylori gastritis. The biopsies showed H. pylori-positive gastritis in 30 children, 9 had gastritis not associated with H. pylori, and 41 had normal biopsies. Atrophic gastritis was not found. The sensitivity and specificity of HPAB for H. pylori were 47% and 98% (cutoff, 38 IU), and 73% and 85% (cutoff, 15 IU), respectively. The assays of pepsinogens and gastrin did not improve sensitivity. None of the markers of pepsinogen (PG) I, PGII, and gastrin 17 (G17) indicated atrophic gastritis. GastroPanel is too insensitive for H. pylori screening and does not replace endoscopy. Markers indicative of atrophic gastritis were negative in all children with H. pylori gastritis.

Topics: Adolescent; Antibodies, Bacterial; Child; Child, Preschool; Endoscopy; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Infant; Pepsinogen A; Reagent Kits, Diagnostic

Previously we showed that a probiotic combination with L. rhamnosus GG was beneficial as an adjuvant therapy during H. pylori eradication.. To evaluate whether probiotic combination with LGG adheres to the upper gastrointestinal mucosa and modifies H. pylori colonisation and H. pylori induced inflammation.. Thirteen patients referred for gastroduodenoscopy received a drink consisting of equal doses (2.5x10(9)CFU) of LGG, L. rhamnosus LC705, Propionibacterium freudenreichii JS and Bifidobacterium lactis Bb12 daily. Recovery of probiotics in biopsies (antrum, corpus, duodenum) and faecal samples was evaluated by strain-specific quantitative polymerase chain reaction. H. pylori colonization and gastric inflammation was investigated by urease activity ((13)C-urea breath test), histology and serum pepsinogen I, II and gastrin-17 measurements.. Twelve patients were fully investigated; of these three of the patients had LGG adhering to the biopsies at end of the intervention. Other probiotic strains were not detected, even though the recovery of all individual probiotic strains from the faeces was significantly increased (p<0.01). After the treatment, the level of (13)C-urea breath test (p=0.063) and gastrin-17 (p=0.046) decreased.. The decreases in (13)C-urea breath test and gastrin-17 indicate that the probiotic combination exerts a beneficial effect on gastric mucosa in H. pylori infected patients. LGG showed marginal ability to adhere to the upper gastrointestinal tract mucosa.

Topics: Adult; Aged; Biomarkers; Biopsy; DNA, Bacterial; Feces; Female; Gastric Mucosa; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogens; Probiotics

To investigate the influence of gender, age, site of lesion, disease type and Helicobacter pylori (H. pylori) infection on the human serum gastrin-17 level and to study the diagnostic value of serum gastrin-17 in gastric precancerous lesions and gastric cancer.. Serum gastrin-17 and serum H. pylori IgG antibody were detected by the ELISA method. The different gastric disease groups were confirmed by endoscopy and histopathology.. Among the 3906 serum samples according to the gender, age, site of lesion and the data of different gastric disease groups, the serum gastrin-17 level was markedly higher in people>or=60 years old than that in younger age groups. The serum gastrin-17 level increased progressively in the following order: healthy control group, nonatrophic gastritis group, gastric ulcer group, and the serum gastrin-17 level was higher in the atrophic gastritis with dysplasia group than that without it, the lowest level being in the gastric cancer group. Among the 2946 serum samples matched with the site of the lesion, the serum gastrin-17 level was higher in those with antral diseases than in those with gastric corpus diseases. Among the 3805 serum samples matched with the H. pylori infection data, the serum gastrin-17 level was higher in the H. pylori-positive group than in the H. pylori-negative group.. In people over 60 years of age, the serum gastrin-17 level tends to increase. In subjects with precancerous gastric lesions, it may increase significantly with the progression of gastric disease, and ultimately decrease in gastric cancer. Serum gastrin-17 is a good biomarker to differentiate benign from malignant gastric diseases. The site of the gastric lesions is an important factor affecting the serum gastrin-17 level, whereas H. pylori infection is usually associated with its increment.

Topics: Adolescent; Adult; Age Factors; Aged; Aged, 80 and over; China; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Precancerous Conditions; Retrospective Studies; Stomach Neoplasms

To investigate the associations of serum gastrin-17 (G-17) concentration with helicobacter pylori (Hp) infection.. A (13)C-urea breath and ELISA test to determine the Helicobacter pylori status and to detect the serum gastrin concentration was conducted in 242 villagers in Linqu of Shandong Province, a high gastric cancer prevalence area in China.. Of 242 subjects, 65 of 111 were found Hp-positive in males (58.56%), compared with 65 of 131 in females (49.62%) (chi(2) = 1.932, P = 0.165). The statistical difference was not observed among different age groups (chi(2) = 4.185, P = 0.123). The average level of G-17 among 242 subjects was (24.43 +/- 25.46) pmol/L and it was statistically higher in females (29.87 +/- 28.18) pmol/L than that in males (18.01 +/- 20.11) pmol/L (Z = -3.618, P < 0.001). However, there was no statistical difference found among age groups (chi(2) = 1.948, P = 0.378). The G-17 level in Hp-negative group (35.50 +/- 30.92) pmol/L was observed significantly higher than in Hp-positive group (14.90 +/- 13.79) pmol/L (Z = 5.368, P = 0.0001).. The G-17 concentration was found higher in Hp-negative subjects than in Hp-positive subjects, and higher in female than in male, but no difference was found among age groups.

Topics: Adult; China; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Rural Population; Sampling Studies

Non-invasive methods are advisable for the detection of Helicobacter pylori-related chronic gastritis in pediatric patients. Serum pepsinogens I and II (sPGII and sPGII), gastrin-17 (G-17) and anti-H. pylori antibodies (IgG-Hp) have been proposed as a 'serological gastric biopsy'.. To assess H. pylori infection and to evaluate gastric mucosa status in a pediatric population by means of serological parameters such as sPGI, sPGII, G-17 and IgG-Hp.. 45 consecutively children evaluated for upper gastrointestinal symptoms were analyzed. All children were submitted to upper gastrointestinal endoscopy with biopsies. Serum samples were analyzed for IgG-Hp, sPGII, sPGI and G-17 (Biohit, Helsinki, Finland).. 18 children had H. pylori-related mild or moderate non-atrophic chronic gastritis. They presented significantly higher mean levels of sPGII and of IgG-Hp than negative ones, either under or up to 10 years. sPGI showed significantly increased levels in H. pylori-positive patients only over 10 years. G-17 levels were not different between H. pylori-positive and -negative ones. The best cut-offs of IgG-Hp, sPGII and of product IgG-Hp x sPGII, to identify H. pylori infection, were 30 IU/l, 9 microg/l, and 241 IU/l x microg/l, respectively. The product IgG-Hp x sPGII identified H. pylori infection with a 100% sensitivity, 92% specificity, 90% positive predictive value and 100% negative predictive value. IgG-Hp and IgG-Hp showed a correlation (r = 0.94; p < 0.001).. Combined analysis of sPGII and IgG-Hp antibody levels could be recommended as a non-invasive panel for the assessment of H. pylori-related histological alterations of gastric mucosa in childhood.

Topics: Adolescent; Biomarkers; Biopsy; Child; Child, Preschool; Female; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Male; Pepsinogens

Topics: Adult; Aged; Aged, 80 and over; Biomarkers, Tumor; Chronic Disease; Duodenal Ulcer; Female; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Pyloric Antrum; Retrospective Studies; Stomach Neoplasms; Stomach Ulcer

The authors describe a current approach to the laboratory diagnosis of chronic gastritis, by using the plates of serological tests: pepsinogen I (PG-I), gastrin 17, and antibodies to Helicobacter pylori (HP). These tests and a questionnaire were used to examine 168 persons aged 45-70 years, who were a random population sample. Almost a fourth of the adult population was observed to have pronounced gastric mucosal atrophic changes, which might be associated with the high prevalence of HP infection. The concentration of PG-I is high in the persons infected with HP, its cytotoxic strains in particular, its elevated level servers as a valid marker of peptic ulcer disease and gastroesophageal reflux.

Topics: Aged; Aged, 80 and over; Antibodies, Bacterial; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Sensitivity and Specificity; Serologic Tests

To study trends in morphological changes of gastric mucosa (GM) and its functional characteristics (serum gastrin-17, pepsinogens I and II) in eradication of Helicobacter pylori (HP) in patients with duodenal ulcer (DU).. HP infection was detected with a rapid urease test, morphological study of gastrobiopsies and polymerase chain reaction in 59 patients with DU. The results of HP eradication were assessed two months after the treatment. Morphological study of gastrobiopsies, assays for gastrin-17, pepsinogens I and II in blood serum were made before the treatment and one year after HP eradication.. By the results of eradication two groups were formed: with effective eradication and uneffective eradication of H. pylori. Examination of GM one year after successful H. pylori eradication in DU patients GM inflammation relieved: reduction in polymorphonuclear (by 42.6%), mononuclear (by 29.3%) infiltration and number of lymphocytic follicules (16.8-fold). GM atrophy decreased by 47.8%. In patients with uneffective eradication the above positive changes were not registered. After H. pylori eradication, serum gastrin-17 lowered by 46. 7%, pepsinogen I--by 30.5%, pepsinogen II--by 36.9%. In uneffective eradication this decrease did not occur.. H. pylori eradication leads to positive changes in morphological and functional indices reflecting GM condition.

Topics: Adult; Anti-Bacterial Agents; Biomarkers; Biopsy; DNA, Bacterial; Duodenal Ulcer; Female; Follow-Up Studies; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Intestinal Mucosa; Male; Pepsinogen A; Pepsinogen C; Polymerase Chain Reaction; Treatment Outcome

Acid secretion is intimately associated with most upper gastrointestinal diseases. Helicobacter pylori infection is a major environmental factor modifying acid secretion.. To study the association between the pattern of H pylori gastritis and gastric secretory function in a large number of subjects without specific upper gastrointestinal disease.. Maximal acid output (MAO) was measured in 255 patients with dyspepsia showing normal endoscopy. Activity and severity of gastritis, atrophy and H pylori infection were assessed in body and antral biopsies. The correlations of histological parameters as well as age, sex, height, weight, smoking, serum gastrin, pepsinogen I and II, and their ratio with MAO were determined. Multiple linear regression was used to show the best possible predictors of MAO.. Negative relationships: Body atrophy and body-combined (active and chronic) inflammatory scores showed a potent inverse correlation with MAO (correlation coefficients (CC) 0.59 and 0.50, respectively). Body:antral chronic gastritis ratio and body:antral combined inflammation ratio (both with CC = 0.49) and age (CC = 0.44) were also inversely correlated with MAO. Intestinal metaplasia at both antral and body sites had negative relationships with acid output with CC = 0.23 and 0.20, respectively. Positive relationships: Serum pepsinogen I, body H pylori density:combined inflammation ratio and pepsinogen I:II ratio with CC of 0.38, 0.38 and 0.30, respectively, correlated with MAO. The H pylori density: combined inflammation of both antrum and body positively correlated with MAO (CC = 0.29 and 0.38, respectively). Male sex and patient height also positively correlated with acid output. Modelling showed that body combined inflammatory score, body atrophy, age and serum pepsinogen I are independent predictors of acid output (R(2) = 0.62).. Combination of body gastritis, body atrophy, age and serum pepsinogen I can be used as predictors of acid-secretory state in populations infected with H pylori.

Topics: Adolescent; Adult; Age Factors; Aged; Aged, 80 and over; Antigens, Bacterial; Bacterial Proteins; Biomarkers; Biopsy; Chronic Disease; Female; Gastric Acid; Gastric Acidity Determination; Gastrins; Gastritis; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Linear Models; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Pyloric Antrum

Corpus dominant gastritis and intestinal metaplasia (IM) are considered markers of increased risk of gastric carcinoma. The aim of our study was to determine serum and histologic risk markers of gastric cancer. Antral and corpus histology, pepsinogen and gastrin 17 levels were compared among patients with history of endoscopic mucosal resection (EMR) for early gastric cancer and controls. Serum pepsinogen (PG) and gastrin 17 levels were measured by RIA. There were 53 gastric cancer patients and 75 controls. The scores for IM in each region and atrophy at the lesser curvature of the corpus were significantly higher in the cancer group than in the H. pylori-positive control group. IM at the greater curvature of the corpus and atrophy at the lesser curvature of the corpus were associated with multiple malignant lesions. Although corpus gastritis was associated with an increased risk of gastric cancer (odds ratio [OR] = 3.4; 95% confidence interval [CI] 1.6-7.0) (p = 0.001), the most important marker was the presence of IM at the lesser curvature of the corpus (OR = 15.1; 95% CI 4.3-52.6) (p < 0.001)). The best cut-off points of serum markers for gastric cancer were a PG I concentration of 45 ng/mL or less and a gastrin 17 >60 pg/mL (sensitivity = 83%; specificity = 68%). IM at the lesser curvature of the corpus and the combination of serum gastrin 17 and PG I identified a group at high risk for development of gastric cancer. Annual endoscopic follow-up is warranted for patients with IM found at the greater curvature of the corpus.

Topics: Aged; Biomarkers; Case-Control Studies; Endoscopy; Female; Gastric Mucosa; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Intestinal Mucosa; Male; Metaplasia; Pepsinogen A; Pepsinogen C; Pyloric Antrum; Stomach Neoplasms

Helicobacter pylori-associated atrophic gastritis is known to be a significant risk factor for gastric cancer. Among the well-known parameters of atrophic gastritis are the levels of serum gastrin-17 (G-17) and pepsinogen I (PG1), which are biomarkers of gastric antral and corpus mucosal activity, respectively. The aim of study was to compare the production of G-17 and PG1 in patients with or without stomach mucosal atrophy and to investigate the utility of serum PG1 and/or G-17 concentrations for the objective evaluation of atrophic gastritis.. A total of 178 dyspeptic Helicobacter pylori-positive patients underwent diagnostic upper gastrointestinal endoscopy with biopsy. The degree of histologic gastric mucosal atrophy was compared with the fasting levels of PG1, and to the postprandial levels of G-17 detected by enzyme immunoassay.. A decrease in serum G-17 levels along with worsening of the antral atrophy was observed; the serum levels of PG1 were reduced during progression of the corpus atrophy. In the multifocal atrophic gastritis, values for PG1 and G-17 serum concentrations were significantly lower than the respective cut-off values. Statistical analysis revealed statistically significant differences between the serum levels of PG1 and G-17 measured at different stages of stomach mucosal atrophy.. A strong reverse correlation was found between histologic/ endoscopic antral atrophy and serum G-17 levels, and between corpus atrophy and serum PG1 levels.

Topics: Adult; Aged; Aged, 80 and over; Antibodies, Bacterial; Biomarkers; Biopsy; Endoscopy, Digestive System; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoenzyme Techniques; Middle Aged; Pepsinogen A; Pyloric Antrum; Sensitivity and Specificity; Severity of Illness Index

Cell division is brisk in the ulcer margin and many of the new cells will migrate over and cover the ulcer bed. The aim of this study was to determine how agents that promote or delay gastric ulcer healing influence cell proliferation in the gastric epithelium.. Acetic acid ulcers were produced in the rat gastric corpus; non-ulcer rats served as controls. All rats were given a continuous infusion of (3)H-thymidine. Some rats were also given gastrin or indomethacin, or infected with Helicobacter pylori. The rats were killed after 1, 2, 6 or 13 days, and the ulcer margin and undamaged corpus were excised for determination of labeling index (LI) by autoradiography. Antrum, duodenum and colon were also studied. Silver grain counting was carried out in some groups.. LI in the ulcer margin grew exponentially, reaching 84% after 6 days; gastrin increased, and indomethacin decreased LI significantly. In 6-day ulcer rats that were given 3H-thymidine only during the first day LI was 5%, while in those given 3H-thymidine only during the last day LI was 27%. LI and silver grain counting results indicated that during the first 6 days of healing the epithelial cells in the ulcer margin divide twice. In the undamaged epithelium of the 1-day ulcer rats LI was

Topics: Acetic Acid; Animals; Anti-Inflammatory Agents, Non-Steroidal; Cell Proliferation; Epithelial Cells; Female; Gastric Mucosa; Gastrins; Helicobacter Infections; Indomethacin; Rats; Rats, Sprague-Dawley; Stomach Ulcer; Thymidine; Wound Healing

To evaluate serum pepsinogen I (PG I) and gastrin-17 (G-17) levels in patients with Helicobacter pylori (H. pylori)-associated chronic atrophic gastritis, with reference to endoscopical Kimura-Takemoto's staging, chromoendoscopical and histological features.. 267 dyspeptic H. pylori-infected patients were examined by chromoendoscopy with biopsy sampling according to the Sydney System and according to Kimura-Takemoto's scale. Simultaneous assessment of serum pepsinogen I (PG I) and gastrin-17 (G-17) levels by enzyme immunoassay was performed. The serologic and morphologic results were compared with correlation analysis.. There was strong reverse correlation between the stomach mucosal atrophy (antral part or corpus) and the proper serologic markers (respectively, G-17 or PG I) in H. pylori-associated chronic gastritis when gastric biopsies taken according to the Sydney System were assessed. The use of Kimura-Takemoto's scale has revealed the decrease of serum PG I levels only at 0-2 and 0-3 grades of the corpus mucosa atrophy. Probably, these results reflects the development of functional failure of the stomach corpus mucosa at late stages of atrophy when its compensatory capacity becomes insufficient. There were not any advantages in sampling biopsies for the detecting of intestinal metaplasia (IM) by the Sydney System, or by Kimura-Takemoto's scheme. The obvious concordance between histologically proven extent of IM and the number of IM foci detected by chromoendoscopy has been revealed.. The biopsy sampling for the diagnosis of precancerous changes of the stomach mucosa after non-invasive screening of atrophic gastritis (e.g., by means of EIA) should be based preferably on the visual signs acquired via chromoendoscopy than through routine endoscopy, independently of the scheme of examination of stomach mucosa, either according to the Sydney System, or to the Kimura-Takemoto's scale.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Atrophy; Endoscopy; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoenzyme Techniques; Male; Middle Aged; Pepsinogen A

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.

Topics: Atrophy; Biomarkers; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Multivariate Analysis; Pepsinogen A; Reproducibility of Results; Single-Blind Method; Stomach

Topics: Child; Diagnosis, Differential; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Pepsinogen A; Pepsinogen C; Sensitivity and Specificity

To detect the Helicobacter pylori (H. pylori)-induced gastric precancerous lesions leading to cancer formation, and to evaluate the possibility of non-invasive screening of dyspeptic patients to identify those having high risk of gastric cancer.. 178 consecutive H. pylori-positive dyspeptic patients after assessment of serum pepsinogen-1 (PG-1) and gastrin-17 (G-17) levels by enzyme immunoassay were examined with endoscopy and histology. The serologic and morphologic results were compared with estimating the sensitivity, specificity and prognostic values of the tests.. There was statistically significant reverse dependence between the presence and severity of stomach mucosal atrophy (in antrum or corpus) and the proper serologic markers of stomach functional activity (G-17 or PG-1). On the other hand, the presence and the degree of intestinal metaplasia, dysplasia and gastric cancer did not correspond to the serum levels of G-17 or PG-1. The serologic method was quite sensitive in the diagnosis of non-atrophic and severe antral and corpus gastritis. Also, it was characterized by the high positive and negative prognostic values. Additionally, we have established the obvious advantage of the chromoendoscopy method in the diagnosis of intestinal metaplasia in the stomach epithelium.. The assays of serum G-17 and PG-1 levels can be offered as the screening tool for atrophic gastritis. The positive serologic results require further chromoendoscopic examination with mucosal biopsy to disclose the probable progression of atrophic process with development of intestinal metaplasia, dysplasia or gastric cancer.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Atrophy; Female; Gastric Mucosa; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Precancerous Conditions; Predictive Value of Tests; Risk Factors; Sensitivity and Specificity; Stomach Neoplasms

Relatives of patients with gastric cancer are at increased risk of developing this disease, especially if they are infected by Helicobacter pylori. Moreover, H. pylori-related atrophic gastritis and hypochlorhydria are well-documented risk factors for noncardia gastric cancer. Serum pepsinogen I (sPGI) and II (sPGII) levels are low in this condition. The aim of our study was to assess by means of a 'Gastropanel' blood test, including sPGI, sPGII, gastrin-17 (G-17) and antibodies anti-H. pylori (IgG-Hp). both functional and morphological features of gastric mucosa in Hp + ve subjects with a family history of gastric cancer.. Twenty-five Hp + ve subjects consecutively referred to our department for gastrointestinal complaints, selected as first-degree relatives of patients suffering from gastric cancer, were enrolled in the study and then matched for sex and age with 25 dyspeptic and Hp + ve subjects with no family history of gastric neoplasia. Blood samples were taken for determination of gastropanel in all patients; in addition, antibodies against CagA were analysed.. No statistically significant differences were detected between the two groups as regards alcohol consumption, coffee intake and smoking habits. Mean sPGI levels in Group A (83.4 +/- 58.4 microg/L) were significantly lower than those in Group B (sPGI 159.5 +/- 80.6 microg/L; P < 0.0001) as well as sPGII (12.5 microg/L = 6.24 versus 20.6 +/- 58 microg/L; P < 0.006). No statistical difference was found between the two groups in relation to G-17 levels, IgG-Hp titres and antibodies against CagA.. First-degree relatives of patients with noncardia gastric cancer affected by H. pylori infection present lower sPGI and sPGII levels, possibly due to the increased frequency of atrophic lesions in these patients.

Topics: Adult; Aged; Aged, 80 and over; Antibodies, Bacterial; Antigens, Bacterial; Bacterial Proteins; Biomarkers; Dyspepsia; Family Health; Female; Gastrins; Gastritis, Atrophic; Genetic Predisposition to Disease; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Stomach Neoplasms

Helicobacter pylori infection is often diagnosed with non-endoscopic methods, such as serology or breath or antigen stool tests. These tests provide information on the presence or absence of the H. pylori gastritis only. We investigated whether atrophic gastritis can be diagnosed and typed non-endoscopically if the serum levels of pepsinogen I (S-PGI) and gastrin-17 (S-G-17) are assayed in connection with H. pylori testing.. The present investigation is an observational case-control study comprising 100 selected dyspeptic outpatients with (cases) or without (controls) advanced (moderate or severe) atrophic gastritis. Before the blood tests, all patients underwent a diagnostic gastroscopy with multiple biopsies. The series of cases includes 56 patients. Eight had an advanced antrum limited atrophic gastritis, 13 had resected antrum (in two of whom the corpus mucosa in the stump was atrophic), and 30 had corpus-limited atrophic gastritis. Four patients had an advanced atrophic gastritis in both the antrum and corpus (multifocal atrophic gastritis), and the whole stomach was removed in one patient. Twenty of the 44 controls had a non-atrophic H. pylori gastritis. Both the antrum and corpus were normal and healthy in 24 patients. The S-PGI and S-G-17 were determined with EIA methods using monoclonal antibodies to PGI and amidated G-17. Postprandial S-G-17 (S-G-17prand) was measured 20 min after a protein-rich drink. The H. pylori antibodies were assayed with a polyclonal EIA method.. A low S-PGI (<25 microg/l; an empirical cut-off with best discrimination) was found in 31 of 37 patients (84%) with and in 3 of 63 patients (5%) without corpus atrophy in the biopsy specimens. A low S-G-17prand (<5 pmol/l) was found in all 8 patients with H. pylori-associated antral atrophy and in 11 of 14 patients (79%) with resected antrum but in 3 of 20 control patients (15%) with H. pylori-related non-atrophic gastritis. Median and mean values of both S-G-17prand and S-PGI decreased with increasing grade of antral and corpus atrophy, respectively. Among all patients with atrophic gastritis (multifocal atrophic gastritis, or atrophic gastritis limited to antrum or corpus) or resected stomach, 50 of 56 patients (89%; Cl 95%: 81%-97%) had a low S-PGI and/or a low S-G-17prand with positive H. pylori serology. Such low values werc found in 3 of the 44 control patients (7%; CI 95%: 0%-14%).. Low serum levels of G-17prand and PGI are conceivable biomarkers of atrophic antral and corpus gastritis, respectively. A low S-G-17prand is a sign of the multifocal or antrum-limited atrophic gastritis in patients infected with H. pylori.

Topics: Antibodies, Bacterial; Antibodies, Monoclonal; Biomarkers; Case-Control Studies; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Sensitivity and Specificity

Hypergastrinemia and a reduction in tissue somatostatin occur in Helicobacter pylori-infected patients. We investigated whether the D cell may be a direct target of gastric inflammation and hypergastrinemia. D cells were quantified by morphometry and flow cytometry in 16-wk-old wild-type (G+/+) and gastrin-deficient (G-/-) mice. Hypochlorhydric G-/- mice were treated with either antibiotics for 20 days or infused with gastrin (G-17) for 14 days. G+/+ mice were made hypochlorhydric by treating them with omeprazole for 2 mo. G-/- mice showed significant inflammation compared with the G+/+ mice, which resolved after 20 days of antibiotic treatment. D cell numbers were not significantly different between G-/- and G+/+ mice. After G-17 was infused, fundic and antral D cell numbers decreased in the G-/- mice. G+/+ animals made hypergastrinemic with omeprazole exhibited decreased D cell numbers. When omeprazole-treated mice were treated with antibiotics alone, elevated plasma gastrin levels returned to baseline and D cell numbers returned to resting levels despite persistent hypochlorhydria. Hypergastrinemia, induced by inflammation, results in decreased D cell numbers. Thus the stomach responds to the presence of inflammation by reducing somatostatin levels, thereby releasing the inhibition on the G and parietal cells to maximize gastric acid output.

Topics: Animals; Anti-Ulcer Agents; Female; Gastric Acid; Gastric Fundus; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Lymphocytes; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Omeprazole; Parietal Cells, Gastric; Pyloric Antrum; Somatostatin

The relationship between plasma gastrin levels and colorectal cancer is controversial. When confounding factors which increase plasma gastrin levels are taken into account, it has been shown that gastrin levels are not elevated in patients with colorectal cancer. However, these studies only measured amidated gastrin. Total gastrin (which includes unprocessed, partially processed, and mature forms of gastrin) has been shown to be elevated in patients with colorectal cancer.. The aim of this study was to determine whether fasting plasma levels of progastrin, amidated gastrin, or glycine extended gastrin are elevated in patients with colorectal cancer or colorectal polyps compared with controls.. Progastrin, amidated gastrin, and glycine extended gastrin were estimated by radioimmunoassay using the following antibodies: L289, 109-21, and L2. Blood samples were analysed for Helicobacter pylori by an enzyme linked immunosorbent assay.. Median progastrin levels were significantly higher in the cancer group (27.5 pmol/l) than in the polyp (< or =15 pmol/l) or control (< or =15 pmol/l) group (p=0.0001 There was no difference in median levels of amidated gastrin between groups. Median levels of amidated gastrin were significantly higher in H pylori positive patients (19 pmol/l) than in H pylori negative patients (8 pmol/l) (p=0.0022). Median plasma progastrin levels were significantly higher for moderately dysplastic polyps (38 pmol/l) compared with mildly dysplastic (15 pmol/l) and severely dysplastic (15 pmol/l) polyps (p=0.05).. Plasma levels of progastrin, but not amidated gastrin or glycine extended gastrin, are significantly elevated in patients with colorectal cancer compared with those with colorectal polyps or controls, irrespective of their H pylori status. We conclude that measuring plasma progastrin levels in patients with colorectal cancer is warranted.

Topics: Adult; Aged; Aged, 80 and over; Antibodies, Bacterial; Biomarkers, Tumor; Carcinoma; Case-Control Studies; Colonic Polyps; Colorectal Neoplasms; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Protein Precursors

To understand the short-term and long-term effects of the eradication of Helicobacter pylori on serum pepsinogen I, gastrin, and insulin concentration, we studied 53 patients with endoscopically proven duodenal ulceration and H. pylori infection.. All patients received a 2-wk course of colloidal bismuth subcitrate, amoxycillin, and metronidazole, and endoscopy was performed at 1.5, 3, 6, and 12 months after entry. H. pylori status was assessed by a urease test and histology.. Among 43 patients in whom H. pylori was eradicated throughout the follow-up year, the mean basal pepsinogen I was 108 ng/ml at pretreatment, decreasing significantly to 85, 77, 80, and 75 ng/ml at 1.5, 3, 6, and 12 months, respectively, at posttreatment. The basal gastrin was 100 pg/ml at pretreatment and fell significantly to 72, 64, 65, and 59 pg/ml, respectively, posttreatment. Of the four patients in whom the H. pylori was not eradicated, there was no significant change in the median basal pepsinogen I and gastrin concentration. Among the six patients in whom the H. pylori was again detectable within the follow-up year, the fallen serum concentration of pepsinogen I and gastrin returned to the pretreatment level. There was no significant change of basal insulin concentration after triple therapy in either the successfully eradicated or failed group.. We conclude that H. pylori is the leading and direct cause of higher serum concentration of pepsinogen I and gastrin in duodenal ulcer patients.

Topics: Amoxicillin; Anti-Ulcer Agents; Bismuth; Drug Therapy, Combination; Duodenal Ulcer; Female; Follow-Up Studies; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Insulin; Male; Metronidazole; Middle Aged; Organometallic Compounds; Pepsinogens; Time Factors

Helicobacter pylori infection increases the serum concentration of gastrin, and this may be one of the mechanisms by which it predisposes to duodenal ulceration. Different forms of circulating gastrin were studied both basally and postprandially in 13 duodenal ulcer patients before and one month after eradication of H pylori. Three antisera that are specific for particular regions of the gastrin molecules were used. Gel chromatography indicated that > 90% of the circulating gastrin consisted of gastrin (G) 17 and G34 both before and after eradicating the infection. The basal median total immunoreactive gastrin concentration fell from 26 pmol/l (range 11-43) to 19 pmol/l (8-39) (p < 0.05), entirely because of a fall in G17 from 6 pmol/l (< 2.4-25) to < 2.4 pmol/l (< 2.4-23) (p < 0.001). The median (range) basal G34 values were similar before (15 pmol (2-36)) and after (10 pmol (2-30)) eradication. The median total immunoreactive gastrin concentration determined 20 minutes postprandially fell from 59 pmol/l (38-114) to 33 pmol/l (19-88) (p < 0.005), and again this was entirely the result of a fall in G17 from 43 pmol/l (9-95) to 17 pmol/l (< 2.4-52) (p < 0.001). The median postprandial G34 values were similar before (13 pmol/l, range 6-42) and after (15 pmol/l, range 6-30) eradication. Eating stimulated a noticeable rise in G17 but little change in G34, both in the presence and absence of H pylori. The finding that H pylori infection selectively increases G17 explains why the infection causes mainly postprandial hypergastrinaemia. G17 is increased selectively because H pylori predominantly affects the antral mucosa which is the main source of G17 whereas G34 is mainly duodenal in origin. This study also indicates that the increased concentration of gastrin in H pylori infection is the result of an increase in one of the main biologically active forms of the hormone.

Topics: Adult; Duodenal Ulcer; Eating; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Protein Precursors

The effect of ulcer healing with eradication of Helicobacter pylori (H pylori) on gastric function was investigated in nine patients with duodenal ulcer disease. One month after eradication there were significant reductions in both basal plasma gastrin concentration, from a median (range) of 19 (1-22) to 6 (2-15) pmol/l (p < 0.05), and of basal acid secretion from 8.3 (2.4-24) to 2.6 (1.4-8.1) mM H+/h, (p < 0.01). The peak acid secretion rate was unchanged from 37 (16-59) to 37 (21-59) mM H+/h. After treatment there was no change in the parietal cell sensitivity to stepped infusions of gastrin heptadecapeptide: the median concentration of gastrin required for 50% of maximal acid secretion (EC50) was 41 (14.8-126) before and 33 (23-125) pmol/l after eradication of H pylori. The metabolic clearance rate of gastrin was also unaffected by the eradication of H pylori. Thus eradication of H pylori infection from patients with active duodenal ulcers is accompanied by falls in both basal gastrin release and basal acid secretion without a change in the parietal cell sensitivity to gastrin. Cyclical changes in H pylori infection may cause the variations in basal acid secretion that are seen in duodenal ulcer disease.

Topics: Acute Disease; Adult; Aged; Bismuth; Drug Therapy, Combination; Duodenal Ulcer; Gastric Acid; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metronidazole; Middle Aged; Organometallic Compounds; Parietal Cells, Gastric; Tetracycline

The effects of age on basal, meal-stimulated, and human gastrin-17-stimulated gastric acid secretion rates and serum pepsinogen concentrations were evaluated in 41 healthy men and women. Older subjects (ages 44-71 years; mean, 57 years) had higher mean basal, meal-stimulated, and gastrin-17-stimulated acid secretory rates and basal serum pepsinogen I and II concentrations than younger subjects (ages 23-42 years; mean, 33 years). Age-related differences in acid secretion were especially prominent in men, and age-related differences in serum pepsinogen I and II concentrations were more prominent in women. Higher gastric acid secretion rates in older subjects could not be explained by body size (height, weight, body surface area, or fat-free body mass) or by the higher incidence of infection with Helicobacter pylori. Using a multivariate linear regression model, age had an independent positive effect on acid secretion, and H. pylori infection had an independent negative effect. It was concluded that aging is associated with an increase in gastric acid secretion in humans, especially in men, while infection with H. pylori is associated with lower acid secretion rates.

Topics: Adult; Aged; Aging; Female; Food; Gastric Acid; Gastrins; Helicobacter Infections; Helicobacter pylori; Hormones; Humans; Male; Middle Aged; Pepsinogens; Regression Analysis