Pepsinogen I Levels Research Articles

B12 deficiency-related glossitis is highly associated with high gastrin-17 and low pepsinogen I.

The causes of vitamin B12 (B12) deficiency are varied and mainly related to gastric disorders. Glossitis is a common oral manifestation of B12 deficiency and is often first seen by dentists. This study aimed to investigate the correlation between B12 deficiency-related glossitis (B12-def glossitis) and gastric serum biomarkers [gastrin-17(G17), pepsinogen I (PGI), pepsinogen II (PGII), and anti-Helicobacter pylori (H. pylori) antibodies], and preliminarily discuss the etiology of B12-def glossitis. A cross-sectional study was conducted in patients complaining of glossodynia, burning sensation, or severe recurrent oral ulcers, but patients with a history of gastrectomy were excluded. All subjects underwent a uniform oral examination and hematological tests. Of 243 patients, 133 with B12-def glossitis were in the case group, and 110 with other oral mucosal diseases (non-glossitis) and normal B12 levels were in the control group. In the case group, 84.2% (112/133) showed high G17 and low PGI levels (G17hi PGIlow ). Univariate logistic regression showed that G17hi PGIlow was a high-risk factor for B12-def glossitis (OR: 92.44; 95% CI: 35.91, 238.02). Subgroup analyses in the case group showed that the G17hi PGIlow group presented with lower B12 levels and a lower positive rate of anti-H. pylori antibodies compared to the non-G17hi PGIlow group. Gastric serum biomarkers in patients with B12-def glossitis generally showed G17hi PGIlow , suggesting possible atrophy of gastric corpus and fundus mucosa. The G17hi PGIlow and non-G17hi PGIlow groups may represent different etiologies of B12 deficiency.

The application of new gastric cancer screening score system for gastric cancer screening and risk assessment of gastric precancerous lesions in China

Objective: To evaluate the value of new gastric cancer screening score system for risk assessment of gastric precancerous lesions. Methods: A total of 520 patients were enrolled after the examination of endoscopy at Endoscopy Center, Department of Gastroenterology, from June 2018 to December 2021. The patients were divided into three groups according to age, gender, serum helicobacter pylori antibody test, pepsinogen I (PGI), pepsinogen II (PGII), pepsinogen I/II ratio (PGR) and gastrin-17 test results before endoscopy: Group A defined as low-risk group (0-11 points), Group B defined as middle-risk group (12-16 points), Group C defined as high-risk group (17-23 points). The detection rates of gastric cancer and atrophic gastritis in three groups were analyzed. According to the range and degree of atrophy/intestinal metaplasia, patients were divided into five groups on the basis of OLGA/OLGIM staging system. The levels of PG I, PG II and PGR were compared between different groups, and the correlation between new gastric cancer screening score system and OLGA/OLGIM staging system were evaluated. Statistical analysis was accomplished by ANOVA, chi-square test and Gamma coefficient analysis. Results: A total of 520 patients were enrolled. 268 patients were classified into group A,222 patients into group B and 30 patients into group C, respectively. According to the pathological results, 281 cases were non-atrophic gastritis, 230 cases atrophic gastritis and 9 cases gastric cancer. For OLGA staging system, 281 patients were divided into stage-0 group, 121 patients into stage-I group, 72 patients into stage-II group, 33 patients into stage-III group and 13 patients into stage-IV groups. The PGI and PGR level correlated inversely with the rising OLGA stages (F = 3.028, p = .016, F = 6.036, p < .001). For OLGIM staging system, 252 patients were divided into stage-0 group, 137 patients into stage-I group, 80 patients into stage-II group, 36 patients into stage-III group and 15 patients into stage-IV group. The PGR level correlated inversely with the rising OLGIM stages (F = 3.466, p＝.007). The detection rates of gastric cancer and atrophic gastritis in Group C were much higher than other groups. (X2 = 14.727, p < .001; X2 = 51.280, p < .001). Gamma coefficient analysis showed significant correlations between OLGA/OLGIM and the new gastric cancer screening score system (p < .001). Conclusions: The new gastric cancer screening score system is closely linked with histological OLGA/OLGIM staging system in the risk assessment of gastric precancerous lesions. The role of new gastric cancer screening score system in future gastric precancerous lesions screening and high risk population identifying was promising.

Determining Gastric Cancer-Related Risk Factors in Mongolian Population Using ABC(D) Method: A Matched Case-Control Study

Objective:We aimed to identify gastric cancer-related risk factors and evaluate the efficacy of screening ABC(D) method in determining high risk gastric cancer individuals in Mongolian population. Methods: A total of 240 participants (120 gastric cancer patients and 120 healthy individuals) were included in this study. Data were collecting using a structured questionnaire consisting of 56 questions covering 5 categories. Serum Helicobacter pylori IgG (H. pylori IgG), pepsinogen I (PGI), and pepsinogen II (PGII) were tested in one third of all the participants (40 gastric cancer patients and 40 controls). PGI, PGII, and H. pylori IgG levels were measured using GastroPanel enzyme-linked immunosorbent assay kit (Biohit, Helsinki, Finland). Results:Habits of having leftover meals (OR 2.22, 95%CI 1.27-3.86, p<0.01), daily consumption of tea with salt (OR 1.97, 95%CI 1.18-3.30, p<0.01), smoking on an empty stomach (OR 2.44, 95%CI 1.11-5.37, p<0.05), daily consumption of vegetables (OR 0.45, 95%CI 0.27-0.76, p<0.01), and daily consumption of fruit juice (OR 0.36, 95%CI 0.15-0.85, p<0.05), family history of gastric cancer (parents OR 2.88, 95%CI 1.07-7.78, p<0.05, siblings (OR 3.09, 95%CI 1.09-8.81, p<0.05), and history of gastric diseases (OR 3.65, 95%CI 2.10-6.35, p<0.0001) were identified as protective factors. A low PGI level (<35.25ng/ml) and low PGI/II ratio (<4) were associated with gastric cancer risk. According to ABC(D) method, groups C and D had higher proportion of gastric cancer cases than group A and B (group C, OR 7.50, 95%CI 1.20-47.05, p<0.05; group D, OR 8.3, 95%CI 1.33-51.26, p<0.05). Conclusion: Our findings suggested that gastric cancer risk was more closely related to eating habits, smoking, family history, and precancerous lesions. ABC(D) method seems to be a plausible alternative or supplementary method for stratifying patients at high risk of gastric cancer in this country.

Effect of Helicobacter pylori eradication therapy on clinical and laboratory biomarkers associated with gastric damage in healthy school-aged children: A randomized non-blinded trial.

Helicobacter pylori (H.pylori) is the primary cause of gastric cancer and eradication in healthy adults has proven effective in decreasing cancer incidence. H.pylori is acquired largely in early childhood, however, the benefits of eradication in children are controversial. We aimed to determine the effect of H.pylori eradication on clinical and laboratory markers associated with gastric damage in apparently healthy school-aged children. This was a pilot non-blinded trial including 61 children persistently infected with H.pylori who were randomized to eradication/no treatment and followed for at least 12months, evaluating clinical and blood markers (Pepsinogen I (PGI) and II (PGII) determined by ELISA) associated with gastric damage. The treatment consisted of a sequential scheme including 7days of omeprazole+amoxicillin followed by 7days of omeprazole+clarithromycin+metronidazole; adherence and tolerance were surveyed. Eradication rates were assessed by stool antigen detection or urea breath test 1month following treatment every 4months thereafter to detect reinfection. Eradication occurred in 30/31 treated children (median age: 8.8, range: 7.9-10.8) and in 0/30 non-treated controls (median age: 8.6, range: 7.9-11) (p<.001). Treatment was associated with mild transient symptoms (altered taste, nocturnal upper abdominal pain, nausea, and diarrhea). Baseline frequency of symptoms was low and eradication did not change symptoms compared to controls. PGI, PGII, and anti-H.pylori seropositivity were similar in both groups at baseline and significantly decreased only in eradicated patients; PGI (92.5 vs. 74.4, p<.001), PGII (15.2 vs. 8.9, p<.001) levels, and frequency of anti-H.pylori seropositivity (100 vs. 68%, p<.001) respectively. Four eradicated children (13%) were reinfected during follow-up. H.pylori eradication therapy in apparently asymptomatic school-aged children was well tolerated and associated with decreased serum PGI and PGII levels. Future studies should expand on the middle-long-term effect of early H.pylori eradication, especially on preventing gastric cancer.

Serum exosomal miR-122-5p, GAS, and PGR in the non-invasive diagnosis of CAG.

ObjectiveThe aim of this study was to integrate the serum exosomal miRNA miR-122-5p with canonical serological biomarkers for the non-invasive screening of chronic atrophic gastritis (CAG) patients.MethodsmiR-122-5p and U6 were amplified by the quantitative reverse transcription polymerase chain reaction (RT-qPCR), gastrin (GAS), pepsinogen I (PG-I), and PG-II and were measured by ELISA. The area under the receiver operating characteristic (ROC) curves and their correlation were analyzed.ResultsIn the present study, GAS level and PG-I/PG-II ratio (PGR) were increased in CAG group, but there was no significant difference in PG-I or PG-II levels between CAG group and chronic non-atrophic gastritis (CNAG) group. Only GAS level and PG-I/PG-II ratio were significantly correlated with atrophy, and not any other clinicopathologic factors. Expression of hsa-miR-122-5p positively correlated with GAS level, PG-I level, and PGR, while it negatively correlated with PG-II level; however, none of them had significant difference. The combination of GAS, PGR, and hsa-miR-122-5p presented as a better model for non-invasive screening of CAG compared to others.ConclusionThese results suggested that serum exosomal hsa-miR-122-5p combined with GAS and PGR would elevate accuracy and specificity in non-invasive screening of CAG.

Expression and clinical significance of paired- related homeobox 1 and Smad2 in gastric cancer.

China has a high incidence rate and low survival rate of gastric cancer. Therefore, there is a great need to further identify novel oncogenes and clinically applicable molecular targets for the diagnosis and treatment of this disease. Expressions of PRRX1, Smad2, epithelial phenotype marker E-cadherin, and interstitial phenotype vimentin protein in a sample of 64 gastric carcinoma and adjacent nontumorous tissues were detected by immunohistochemistry. Their relationship and correlations with clinicopathological features were analyzed. The positive rates of PRRX1, Smad2, E-cadherin, and vimentin protein in primary tumors were 60.94% (39/64), 59.38% (38/64), 34.38%(22/64), and 64.06% (41/64), respectively. A significant correlation was found among the expression of PRRX1, Smad2, E-cadherin, and vimentin (P < 0.05). Expression of the PRRX1, Smad2, and vimentin protein in gastric cancer tissue was correlated with Borrmann classification, lymph node-positive number, the degree of differentiation, depth of tumor invasion, and serum pepsinogen I (PGI) level (P < 0.05), but not with age, sex, serum carcinoembryonic antigen, serum CA199, or PGI/PGII (P > 0.05). The positive rate of PRRX1 protein expression was positively correlated with the protein expression of Smad2 and vimentin, but negatively correlated with E-cadherin protein. PRRX1, Smad2, and vimentin proteins are associated with Borrmann type, lymph node positives, histologic grade, depth of tumor invasion, and serum PGI levels, all of which contribute to a poor prognosis for patients with gastric cancer.

Associations of Serum Pepsinogens and Helicobacter Pylori Infection with High-Sensitivity C-Reactive Protein in Medical Examination Population.

This study aimed to clarify the distribution characteristics of serum pepsinogen (PG) and Helicobacter pylori in the medical examination population and to explore the relationships of PG level and H. pylori infection status with the high-sensitivity C-reactive protein (hsCRP) level and their significance in health examination. We detected H. pylori infection by C13 urea breath test, the serum pepsinogen I (PGI) and pepsinogen II (PGII) contents were measured by chemiluminescence microparticle immunoassay, and the PGI/PGII ratio was calculated. In addition, the serum hsCRP level was determined by the Abbott C16000 automatic biochemical analyzer. The PGI and hsCRP levels were significantly higher in men than in women, and the PGII level was slightly higher in men than in women (both P <.05). The PGI, PGII, and hsCRP levels were positively correlated with age (r = 0.210, 0.287, and 0.133, respectively; P <.05), whereas the PGI/PGII ratio was negatively correlated with age (r = -0.190; P <.05). The positive H. pylori infection rate was 30.2% among the patients in this study; H. pylori infection was not related to sex (P >.05), and the difference in age stratification was not statistically significant (P >.05). The abnormal PGI/PGII ratio in the medical examination population was not correlated with sex (P >.05). In the H. pylori positive infection group, the proportion of PGI/PGII ratio <3, the PGI and PGII levels were significantly higher than those in the H. pylori negative infection group, and the PGI/PGII ratio was significantly lower than that in the negative group (both P <.05). The hsCRP level was not associated with H. pylori infection (P >.05), and it was significantly higher in the PGI/PGII ratio <3 group than in the PGI/PGII ratio ≥3 group (P <.05). The PGI and PGII levels and the PGI/PGII ratio are correlated with H. pylori infection. The abnormal PGI/PGII ratio is closely related to H. pylori infection and hsCRP level. Therefore, H. pylori infection status and hsCRP level should be considered when determining atrophic gastritis by the PGI/PGII ratio.

Changes in serum pepsinogen levels and their value as a predictor of treatment outcomes in children with peptic ulcer.

To investigate pepsinogen secretion from the neonatal stage to childhood and its diagnostic value for peptic ulcer (PU) in children. In this study, 2114 'healthy' children and 51 children with PUs undergoing a medical examination by gastroscopy were selected as subjects. The serum content of pepsinogen I (PGI) and serum pepsinogen II (PGII) was tested for each of the subjects using time-resolved fluorescence immunoassay, which is characterised by high sensitivity and a wide measuring range. The serum PGI and PGII levels were found to increase with age, becoming stable and similar to those of adults at the age of 16. In 51 children with PUs, PGI was 201.03 ± 30.74 ng/mL before treatment and 187.92 ± 19.86 ng/mL after treatment (P > 0.05); PGII was 17.36 ± 1.47 ng/mL before treatment and 17.20 ± 3.98 ng/mL after treatment (P > 0.05). It is difficult to establish the normal range of PG in children owing to its variance by age. However, if the normal reference range for individual age groups is known, it may still serve as a useful diagnosis system as well as a detecting indicator during the course of PU treatment. There are significant differences in PGI expression in children with PU before and after PU is cured, whereas other indicators show no differences before and after treatment.

Influence of laboratory-related and endoscopy-related factors on the assessment of serum pepsinogens and gastrin-17.

Serum pepsinogen I (PGI) and pepsinogen II (PGII) are noninvasive parameters in the detection of atrophic gastritis. The diagnostic add-on value of serum gastrin-17 (G-17) remains uncertain. The aim of this study was to assess the stability of these serum parameters over time and to evaluate the influence of clinical factors, such as upper gastrointestinal (GI) endoscopy and bowel cleansing, on serum PGI, PGII, and G-17 assessment. A prospective study was carried out in healthy individuals and patients. For the stability analyses, the plasma and serum samples from 23 individuals were processed at different time points with and without the addition of a stabilizer. Ten patients were included to evaluate the influence of upper GI endoscopy and 18 patients to evaluate the effect of bowel cleansing before colonoscopy. PGI, PGII, and G-17 levels were not statistically different in the serum and plasma. PGI and PGII serum levels were stable over time. G-17 is associated with time-dependent degradation (P=0.0001). The addition of the G-17 stabilizer showed no improvement in stability. Upper GI endoscopy and bowel preparation before colonoscopy were associated with minimal variations in PGI and PGII, whereas G-17 showed patient-specific alterations. PGI and PGII serum levels are stable over time. However, G-17 stability is strongly dependent on the time of processing and storage; therefore, samples for G-17 analysis need to be processed no later than 6 h after blood collection. Upper GI endoscopy and colonoscopy preparation lead to minimal nonsignificant changes in basal PGI, PGII, and G-17 levels.

Abstract 5304: A serological biopsy using five stomach-specific circulating biomarkers for gastric cancer risk assessment: a multi-phase study

Abstract Objective: We aimed to assess a serological biopsy using five stomach-specific circulating biomarkers—pepsinogen I (PGI), PGII, PGI/II ratio, anti-Helicobacter pylori (H. pylori) antibody, and gastrin-17 (G-17)—for identifying high-risk individuals and predicting risk of developing gastric cancer (GC). Methods: Among 12112 participants with prospective follow-up from an ongoing population-based screening program using both serology and gastroscopy in China, we conducted a multi-phase study involving a cross-sectional analysis, a follow-up analysis, and an integrative risk prediction modeling analysis. Results: In the cross-sectional analysis, the five biomarkers (especially PGII, the PGI/II ratio, and H. pylori sero-positivity) were associated with the presence of precancerous gastric lesions or GC at enrollment. In the follow-up analysis, low PGI levels and PGI/II ratios were associated with higher risk of developing GC, and both low (&amp;lt;0.5 pmol/L) and high (2.0-4.7 or &amp;gt;4.7 pmol/L) G-17 levels were associated with higher risk of developing GC, suggesting a J-shaped association. In the risk prediction modeling analysis, the five biomarkers combined yielded a C statistic of 0.801 (95% CI=0.787-0.815) and improved prediction beyond traditional risk factors (C statistic from 0.580 to 0.811, P&amp;lt;0.001) for identifying precancerous lesions at enrollment, and higher serological biopsy score based on the five biomarkers at enrollment were associated with higher risk of developing GC during follow-up (P for trend &amp;lt;0.001). Conclusions: A serological biopsy composed of the five stomach-specific circulating biomarkers could be used to identify high-risk individuals for further diagnostic gastroscopy, and to stratify individuals’ risk of developing GC and thus to guide targeted screening/precision prevention. Citation Format: Huakang Tu, Liping Sun, Xiao Dong, Yuehua Gong, Qian Xu, Jingjing Jing, Roberd M. Bostick, Xifeng Wu, Yuan Yuan. A serological biopsy using five stomach-specific circulating biomarkers for gastric cancer risk assessment: a multi-phase study [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 5304. doi:10.1158/1538-7445.AM2017-5304

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

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

Serum Indicators Reflecting Gastric Function May Also Correlate with Other Extragastric Diseases.

Aim. Serological indicators of organ function can reveal intrinsic links between different organs. The present study aimed to determine the correlations of serum indicators for gastric and extragastric function. Methods. A total of 823 individuals were enrolled. Data on indicators reflecting blood lipids, blood glucose, indexes of stomach, kidney, liver, and thyroid function, and H. pylori IgG antibody level were collected. Results. As creatine (Cr) levels increased, PGI (pepsinogen I), PGII concentrations, and PGI/II ratio increased monotonically from 79.7 to 105.15 µg/L, 6.5 to 8.4 µg/L, and 11.97 to 12.27, respectively (P < 0.05). As thyroid peroxidase antibody (TPOAb) levels increased, PGI level decreased from 100.85 to 84 µg/L (P < 0.05) and as thyroid stimulating hormone (TSH) increased, PGI/II ratio increased monotonically from 11.54 to 12.68 (P < 0.05). As triglyceride (TG) levels increased, gastrin 17 (G17) concentrations increased monotonically from 1.73 to 2.7 pmol/L (P < 0.05). As serum glucose and glycated hemoglobin (HbA1C) increased, PGI/II concentrations increased monotonically from 11.98 to 12.67 and 9.7 to 13.54 (P < 0.05), respectively. Conclusions. Serum PG and G17 levels were associated with blood glucose and lipids, kidney function, and thyroid function but not with liver function. Serum indicators reflecting gastric function may correlate not only with primary diseases, but also with other extragastric diseases.

Niveles séricos de pepsinógeno y su capacidad diagnóstica de atrofia gástrica en diferentes poblaciones colombianas

ObjectiveTo characterize levels of pepsinogen and evaluate the discrimination ability of pepsinogen I (PGI) and the PGI/ pepsinogen II (PGII) ratio for the serological diagnosis of gastric atrophy in different Colombian populations. MethodsA total 600 subjects without gastric symptoms participated and 544 samples from patients with gastric symptomatology were analyzed from different populations with opposing risks to gastric cancer. A blood sample was taken from all participants; a gastric antrum and body biopsy for the initial diagnosis of gastroduodenal lesions was obtained from the patients. The levels of pepsinogen and Helicobacter pylori serology were estimated with ELISA. Statistical analyses included Kruskal -Wallis and Mann -Whitney test, ROC curve and diagnostic values. ResultsThe levels of PGI and PGI / PGII differ by risk area of origin. Levels of PGI, PGII and PGI / PGII decreased with increasing severity of histological diagnosis (P<.005), as with the severity of atrophy and multifocal localization (P ≤.001). The PGI ≤ 86.68 and PGI / PGII ≤ 3.19 with an area under the curve of 0.76 identified patients with severe multifocal atrophy, positive serology for H. pylori, and from the high risk area, with a sensitivity of 77.5% and specificity of 71.74%. ConclusionThe results suggest that PGI levels together with PGI / PGII ratios and positive serology for H. pylori could be considered for the detection of severe atrophy in high-risk areas. Further studies are needed in high-risk populations

Patients with Helicobacter pylori infection have less severe gastroesophageal reflux disease: a study using endoscopy, 24-hour gastric and esophageal pH metry

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.

Association between polymorphisms in glutathione S-transferase Mu3 and IgG titer levels in serum against Helicobacter pylori

This study investigated the association between glutathione S-transferases (GST) polymorphisms and immunoglobin G (IgG) titer levels in serum against Helicobacter pylori (H. pylori). Out of a total 300 healthy subjects seropositive for H. pylori, we analyzed the relationship between 15 single-nucleotide polymorphisms (SNPs), namely two in GST-mu2 (GST-M2), five in GST-mu3 (GST-M3), four in GST-pi1 (GST-P1) and four in GST-theta2 (GST-T2), and IgG antibody titer levels in serum against cytotoxin-associated gene A (CagA) and the surface antigen of H. pylori (Hp), as well as the levels of pepsinogen I (PGI). Titer levels were classified by tertile. The age-sex adjusted odds ratios (ORs) and 95% confidence intervals (CIs) in the middle and low titer groups were calculated using a polytomous logistic regression model, with the high titer group considered as control. Results for GST-M3 showed a significant association between SNPs, CagA and Hp titers. In addition, the AA genotype (high enzyme activity) from SNP rs7483 (Val224Ile) in GST-M3 showed a significantly low risk for being in the low titer group (OR: 0.48, 95% CI: 0.27-0.86 and OR: 0.46, 95% CI: 0.26-0.83 for CagA and Hp, respectively). Furthermore, the AA genotype from the rs7483 SNP showed significantly (P<0.05) higher PGI levels than did the genotypes harboring a G allele (mean (s.d.)=66.9 (32.0) and 59.1 (30.7) microg ml(-1) for AA and AG+GG, respectively). Our results suggest that GST-M3 polymorphisms are associated with levels of IgG titer in serum against H. pylori. GST-M3 activity is possibly involved in protection against mucosal atrophy caused by H. pylori as the levels of IgG titer and PGI are linked to mucosal status.

Early Changes in Ghrelin following Roux-en-Y Gastric Bypass: Influence of Vagal Nerve Functionality?

Roux-en-Y gastric bypass (RYGBP) effectively produces massive weight reduction, improving health in morbidly obese patients. The mechanisms for the weight loss, and the fate of the excluded gastric mucosa, are not fully clarified. To what extent the appetite-stimulating gastric peptide ghrelin is affected remains controversial. Circulating concentrations of ghrelin, pancreatic polypeptide (PP), pepsinogen I (PGI) and gastrin were examined in 15 morbidly obese patients (median BMI 45 kg/m2) preoperatively, and on days 1, 2, 4, 6 and at months 1, 6 and 12 after RYGBP. Ghrelin levels fell on postoperative day 1 and increased after 1 month to preoperative levels, and rose further at 6 and 12 months. PP concentrations decreased on day 1 and subsequently returned to preoperative levels. PGI levels peaked transiently the first days after surgery and subsequently declined to lower than preoperative levels. Gastrin levels were gradually reduced postoperatively. Ghrelin and PP fall transiently after surgery, possibly due to vagal dysfunction, and ultimately, as weight loss ensues, ghrelin secretion increases to higher than preoperative levels. The RYBGP procedure affects the gastric mucosa, as reflected by a transient increase in circulating PGI, and subsequently, the mucosa in the excluded stomach is at rest, as shown by low levels of PGI and gastrin.

Prediction of gastroesophageal reflux in otitis media with effusion in adults

Conclusions. The measurement of pepsinogen I (PGI) in middle-ear effusions (MEEs) and a questionnaire on the frequency symptoms of gastroesophageal reflux (GER) disease are tools that can be used to screen for the existence of GER. Objective. To seek methods that would be beneficial as a screen for the presence of GER among adult patients with OME. Materials and methods. Fifty-eight adult outpatients with OME were asked to answer a questionnaire of the frequency scale for symptoms of GER disease. Samples of MEEs were obtained from each subject and were measured for concentrations of PGI and PGII. Some patients were followed up after being treated with a proton pump inhibitor. Results. The percentage of patients with high PGI concentrations in their MEEs was higher in those with GER-related symptoms than in those without GER-related symptoms. Moreover, OME was present bilaterally in a higher percentage of patients with GER-related symptoms. There were patients in whom PGI levels decreased after receiving treatment for GER.

Influence of antisecretory treatment with proton pump inhibitors on serum pepsinogen I levels

It has been reported in literature that serum pepsinogen levels rise during omeprazole and lansoprazole administration. However, the influence of pantoprazole and esomeprazole on serum pepsinogens levels is still to be assessed. The aim of this study was to evaluate the influence of proton pump inhibitor (PPI) therapy on pepsinogen I (PGI) levels. PGI and gastrin (G17) levels (EIA; Biohit, Helsinki, Finland) in 126 consecutive patients (M 57; F 69, mean age 53, range 15-91), with upper gastrointestinal symptoms at baseline condition and after 2 months of PPI treatment, were evaluated. Patients underwent a therapy schedule based on: omeprazole 20 mg b.i.d. (20 patients), pantoprazole 40 mg b.i.d. (27 patients), esomeprazole 40 mg b.i.d. (29 patients), lansoprazole 30 mg b.i.d. (21 patients) and rabeprazole 20 mg b.i.d. (26 patients) for 2 months. A significant increase in serum PGI (sPGI) levels was found after a 2-month treatment for all five different PPIs: omeprazole, pantoprazole, esomeprazole, lansoprazole and rabeprazole (P < 0.05). The effect of rabeprazole on sPGI was less pronounced as compared with other PPIs, whereas esomeprazole achieved superior sPGI levels, with no overall statistically significant difference among the five groups (P > 0.05). However, a comparison within a single group of PPIs showed a statistical significance when the esomeprazole group was compared with the rabeprazole group (P = 0.007). sPGI levels are significantly influenced by antisecretory therapy, rising under PPI treatment. Moreover, a statistically significant difference in sPGI levels between the rabeprazole and esomeprazole groups has been demonstrated.

Serum Progastrin and Its Products, Gastric Acid Secretion and Serum Pepsinogen I in Gastric Cancer

Background: Numerous studies have shown an association between Helicobacter pylori (Hp) infection and gastric cancer (GC). Study: This study was designed to determine the role of cytotoxin-associated gene A (CagA)-positive Hp infection, serum amidated gastrins and their precursor, progastrin, gastric acidity and serum pepsinogen I (PG-I) levels in gastric cancerogenesis in 74 cancer patients and in 77 age- and gender-matched controls. Serum IgG antibodies to Hp and CagA and levels of IL-8 and PG-I were measured by ELISA, while progastrin and amidated gastrin by specific radioimmunoassay. Results: The overall Hp and CagA seropositivity in GC patients were significantly higher (82 and 60%) than in matched controls (61 and 27%, respectively). Progastrin and amidated gastrin levels over their cutoff points (122 and 32 pM, respectively) were found in a significantly larger number of GC (59.4 and 44.5%) than in controls (9.0 and 16.8%, respectively). Histologically, all these GCs with increased serum progastrin and amidated gastrins were of intestinal type and showed CagA and Hp seropositivity. Serum IL-8 and gastric pH, above their cutoff points (pH >4.5), and serum PG-I level below its cutoff point (44.2 µg/l) were observed in a significantly higher number of GC patients as compared to controls. Conclusions: (1) GC patients have higher Hp and CagA seroprevalence than matched controls, confirming that CagA-positive Hp infection is associated with higher risk of GC; (2) serum levels of amidated gastrins and their precursor, progastrin, as well as IL-8 are significantly higher, while serum PG-I levels are reduced in intestinal type GC compared to controls, and (3) determination of high serum progastrin, amidated gastrins and IL-8 combined with low serum PG-I may be useful biomarkers of GC.

Increased serum pepsinogen-I level predicts development of new duodenal erosion following eradication teraphy of H.pylori

Aims: Eradication of Helicobacter pylori (Hp) decreases the concentrations of serum gastrin (G) and pepsinogen (PG). However, the changes in serum level of such peptides during or just after eradication therapy have not been well investigated. In this study, we evaluated the changes in serum G and PG levels at the end of eradication therapy, and then investigated the relation to the duodenal erosion following eradication. Methods: We randomly treated 318 patients (104 female and 318 men, mean age 51 years) with abdominal symptom (109 gastric ulcer (GU), 113 duodenal ulcer (DU), 32 gastro-duodenal ulcer (GDU), and 64 atrophic gastritis (AG». Before eradication, endoscopy was performed and patients with duodenal erosion were excluded. One month after eradication, endoscopy was performed to check duodenal erosion, and Hip culture, histology, and urea breath test performed to assess Hip treatment. We determined G and PG level in sera at three time points: before eradication, at the end of eradication, and one month after eradication. Results: In 272 (85.5%) cured patients, 39 (14.3%) patients had new duodenal erosions. In 46 (14.5%) patients with unsuccessful treatment, no duodenal erosion appeared. Duodenal erosion developed in 27.3%, 10.7%, 9.1%, and 0% in the patients with DU, GDU, GU, and AG. The prevalence of duodenal erosion after Hip eradication was significantly higher (p < 0.005) in DU patients than in GU, and AG patients. In cured patients, G, PG-I, II, and IIII level one month after eradication were significantly decreased compared to those measured before eradication (p < 0.005). At the end of eradication, G and PG-I level were significantly higher than before eradication (p < 0.0001). In uncured patients, no changes were seen. In the patients with new duodenal erosions, G, PG-I, II, and IIII levels were similar to non-duodenal erosion patients before eradication and one month after eradication. However, at the end of eradication, only PG-I levels were significantly higher (p < 0.0001) than in the patients with non-duodenal erosion. Conclusions: 1. Successful Hip treatment causes a temporary high G and PG-I response at the end of eradication therapy. 2. Increased PG-I might be a kind of gastric mucosal response to H.p eradication since this temporary high level of serum PG-I is strongly associated with development of new erosions in duodenum. 3. These phenomenon strongly bring about duodenal mucosal damage by excess acid secretion and PG-I following eradication therapy.