The Experts below are selected from a list of 867 Experts worldwide ranked by ideXlab platform
David Y Graham - One of the best experts on this subject based on the ideXlab platform.
-
noninvasive evaluation of helicobacter pylori therapy role of fasting or postprandial gastrin Pepsinogen i Pepsinogen II or serum igg antibodies
The American Journal of Gastroenterology, 1999Co-Authors: Tarek M Alassi, John H Walsh, Kazumasa Miki, David P Graham, Masahiro Asaka, David Y GrahamAbstract:Noninvasive evaluation of Helicobacter pylori therapy: role of fasting or postprandial gastrin, Pepsinogen I, Pepsinogen II, or serum IgG antibodies
-
original contributionsnoninvasive evaluation of helicobacter pylori therapy role of fasting or postprandial gastrin Pepsinogen i Pepsinogen II or serum igg antibodies
The American Journal of Gastroenterology, 1999Co-Authors: Tarek M Alassi, John H Walsh, Kazumasa Miki, David P Graham, Masahiro Asaka, David Y GrahamAbstract:OBJECTIVE: We evaluated the potential value of a change in serum IgG antibodies, fasting or meal-stimulated gastrin levels, and Pepsinogen I (PGI) or Pepsinogen II (PGII) levels for identifying Helicobacter pylori (H. pylori) status after antibiotic therapy. METHODS: A total of 32 men and one woman with peptic ulcer disease and documented H. pylori infection were enrolled. Fasting and 30-min postprandial blood samples were obtained at 0, 2, 7, 11, 17, 23, 27, and 39 wk of the study and were analyzed for the factors evaluated. RESULTS: Treatment was successful in 25 patients and failed in seven. Serum IgG antibodies, meal-stimulated gastrin, and both fasting and meal-stimulated Pepsinogen I and II levels fell throughout the study, and Pepsinogen I:II ratios increased in those whose infection was cured. The mean levels at wk 0 versus wk 7 were: fasting gastrin (fmol/ml) 12.4 and 11, meal-stimulated gastrin 26.5 and 15.4, PGI (ng/ml) 83.7 and 59, PGII (ng/ml) 24.5 and 13.6, PGI/PGII 3.5 and 4.7, and enzyme-linked immunosorbent assay value 4.8 and 4.55. The sensitivity, specificity, and positive and negative predictive values for the data analyzed using different percent changes (e.g., 80%, 50%, and 20%) were calculated. The specificity and sensitivity remained <80% at all time points. CONCLUSIONS: Despite a significant fall in serum markers of H. pylori infection in groups of individuals, no marker tested could be used to reliably determine posttherapy H. pylori status for individual patients.
Christian C Abnet - One of the best experts on this subject based on the ideXlab platform.
-
Research Article Association between Upper Digestive Tract Microbiota and Cancer-Predisposing States in the Esophagus and Stomach
2016Co-Authors: Mitchell H. Gail, S M Dawsey, Jin-hu Fan, Jianxin Shi, Vanja Klepac-ceraj, Bruce J. Paster, Bruce A. Dye, Neal D. Freedman, Christian C AbnetAbstract:Background: The human upper digestive tract microbial community (microbiota) is not well characterized and few studies have explored how it relates to human health. We examined the relationship between upper digestive tract microbiota and two cancer-predisposing states, serum Pepsinogen I/Pepsinogen II ratio (PGI/II; predictor of gastric cancer risk) and esophageal squamous dysplasia (ESD; the precursor lesion of esophageal squamous cell carcinoma; ESCC) in a cross-sectional design. Methods: The Human Oral Microbe Identification Microarray was used to test for the presence of 272 bacterial species in 333 upper digestive tract samples from a Chinese cancer screening cohort. Serum PGI and PGII were determined by ELISA. ESD was determined by chromoendoscopy with biopsy. Results: Lower microbial richness (number of bacterial genera per sample) was significantly associated with lower PGI/II ratio (P 0.034) and the presence of ESD (P 0.018). We conducted principal component (PC) analysis on a b-diversity matrix (pairwise difference in microbiota), and observed significant correlations between PC1, PC3, and PGI/II (P 0.004 and 0.009, respectively), and between PC1 and ESD (P 0.003). Conclusions: Lower microbial richness in upper digestive tract was independently associated with both cancer-predisposing states in the esophagus and stomach (presence of ESD and lower PGI/II). Impact:These novel findings suggest that the upper digestive tractmicrobiotamayplay a role in the etiology of chronic atrophic gastritis and ESD, and therefore in the development of gastric and esophageal cancers. Cancer Epidemiol Biomarkers Prev; 23(5); 735–41. 2014 AACR
-
AUCs for discrimination of fundic atrophy (dark bar), and nonatrophic pangastritis (dotted bar represents the study population after exclusion of fundic atrophy from reference group, diagonal lined bar represents whole study population).
2013Co-Authors: Dariush Nasrollahzadeh, Farin Kamangar, Christian C Abnet, Karim Aghcheli, Masoud Sotoudeh, Ramin Shakeri, Christina E. Persson, Farhad Islami, Paolo Boffetta, Lars EngstrandAbstract:AUC: Area under curve, PGI: Pepsinogen I, PGII. Pepsinogen II, PGI/PGII ratio: Pepsinogen I/Pepsinogen II ratio, G-17: gastrin-17.
-
Screening characteristics of PGI and PGI/PGII ratio for diagnosis of fundic atrophy and nonatrophic pangastritis.
2013Co-Authors: Dariush Nasrollahzadeh, Farin Kamangar, Christian C Abnet, Karim Aghcheli, Masoud Sotoudeh, Ramin Shakeri, Christina E. Persson, Farhad Islami, Paolo Boffetta, Lars EngstrandAbstract:CI: confidence interval, AUC: area under curve, PPV: positive predictive value, NPV: negative predictive value, PGI: Pepsinogen I, PGII: Pepsinogen II, G-17: gastrin-17.
-
Levels of Pepsinogens, gastrin, and percentage of subjects seropositive for H. pylori, and CagA according to the topography of moderate/marked gastritis and atrophy.
2013Co-Authors: Dariush Nasrollahzadeh, Farin Kamangar, Christian C Abnet, Karim Aghcheli, Masoud Sotoudeh, Ramin Shakeri, Christina E. Persson, Farhad Islami, Paolo Boffetta, Lars EngstrandAbstract:SD: Standard deviation, IQR: interquartile range, PGI: Pepsinogen I, PGII: Pepsinogen II, CagA: cytotoxin-associated gene A, PPI (proton pump inhibitor).*H. pylori status was determined according to the results of histology examination, ELISA IgA/IgG, and Western blot.
-
gastric atrophy and oesophageal squamous cell carcinoma possible interaction with dental health and oral hygiene habit
British Journal of Cancer, 2012Co-Authors: Dariush Nasrollahzadeh, Farin Kamangar, Karim Aghcheli, Farhad Islami, Reza Malekzadeh, M Sotoudeh, Shahin Merat, Christian C AbnetAbstract:Gastric fundal atrophy has been hypothesised to increase the risk of oesophageal squamous cell carcinoma (OSCC), but studies have shown inconsistent results. We measured serum Pepsinogen I (PGI) and Pepsinogen II (PGII) among 293 incident cases and 524 matched neighbourhood controls in a high-risk area of Northern Iran. Conditional logistic regression model was used to estimate odds ratios (ORs) and their 95% confidence intervals (CIs). After controlling for age, sex, residence area and other potential confounders, gastric atrophy (defined by a validated criterion, PGI <55 μg dl−1) was associated with a two-fold increased risk (OR=2.01, 95% CI: 1.18, 3.45) of OSCC in the absence of nonatrophic pangastritis (defined as PGII <11.8 μg dl−1). Stratification by PGII decreased the misclassification errors due to cancer-induced gastritis. Presence of both poor dental health, indicated by higher than median sum of decayed, missing, and filled teeth (DMFT score), and gastric atrophy further increased the risk of OSCC (OR=4.15, 95% CI: 2.04, 8.42) with relative excess risk due to interaction (RERI) of 1.47 (95% CI: −1.15, 4.1). Coexistence of poor oral hygiene habit with gastric atrophy elevated OSCC risk eight times (OR=8.65, 95% CI: 3.65, 20.46) and the additive interaction index was marginally statistically significant (RERI=4.34, 95% CI: −1.07, 9.76). Gastric atrophy is a risk factor for OSCC, and poor dental health and oral hygiene habit may act synergistically in increasing the risk.
Tarek M Alassi - One of the best experts on this subject based on the ideXlab platform.
-
noninvasive evaluation of helicobacter pylori therapy role of fasting or postprandial gastrin Pepsinogen i Pepsinogen II or serum igg antibodies
The American Journal of Gastroenterology, 1999Co-Authors: Tarek M Alassi, John H Walsh, Kazumasa Miki, David P Graham, Masahiro Asaka, David Y GrahamAbstract:Noninvasive evaluation of Helicobacter pylori therapy: role of fasting or postprandial gastrin, Pepsinogen I, Pepsinogen II, or serum IgG antibodies
-
original contributionsnoninvasive evaluation of helicobacter pylori therapy role of fasting or postprandial gastrin Pepsinogen i Pepsinogen II or serum igg antibodies
The American Journal of Gastroenterology, 1999Co-Authors: Tarek M Alassi, John H Walsh, Kazumasa Miki, David P Graham, Masahiro Asaka, David Y GrahamAbstract:OBJECTIVE: We evaluated the potential value of a change in serum IgG antibodies, fasting or meal-stimulated gastrin levels, and Pepsinogen I (PGI) or Pepsinogen II (PGII) levels for identifying Helicobacter pylori (H. pylori) status after antibiotic therapy. METHODS: A total of 32 men and one woman with peptic ulcer disease and documented H. pylori infection were enrolled. Fasting and 30-min postprandial blood samples were obtained at 0, 2, 7, 11, 17, 23, 27, and 39 wk of the study and were analyzed for the factors evaluated. RESULTS: Treatment was successful in 25 patients and failed in seven. Serum IgG antibodies, meal-stimulated gastrin, and both fasting and meal-stimulated Pepsinogen I and II levels fell throughout the study, and Pepsinogen I:II ratios increased in those whose infection was cured. The mean levels at wk 0 versus wk 7 were: fasting gastrin (fmol/ml) 12.4 and 11, meal-stimulated gastrin 26.5 and 15.4, PGI (ng/ml) 83.7 and 59, PGII (ng/ml) 24.5 and 13.6, PGI/PGII 3.5 and 4.7, and enzyme-linked immunosorbent assay value 4.8 and 4.55. The sensitivity, specificity, and positive and negative predictive values for the data analyzed using different percent changes (e.g., 80%, 50%, and 20%) were calculated. The specificity and sensitivity remained <80% at all time points. CONCLUSIONS: Despite a significant fall in serum markers of H. pylori infection in groups of individuals, no marker tested could be used to reliably determine posttherapy H. pylori status for individual patients.
S M Dawsey - One of the best experts on this subject based on the ideXlab platform.
-
Research Article Association between Upper Digestive Tract Microbiota and Cancer-Predisposing States in the Esophagus and Stomach
2016Co-Authors: Mitchell H. Gail, S M Dawsey, Jin-hu Fan, Jianxin Shi, Vanja Klepac-ceraj, Bruce J. Paster, Bruce A. Dye, Neal D. Freedman, Christian C AbnetAbstract:Background: The human upper digestive tract microbial community (microbiota) is not well characterized and few studies have explored how it relates to human health. We examined the relationship between upper digestive tract microbiota and two cancer-predisposing states, serum Pepsinogen I/Pepsinogen II ratio (PGI/II; predictor of gastric cancer risk) and esophageal squamous dysplasia (ESD; the precursor lesion of esophageal squamous cell carcinoma; ESCC) in a cross-sectional design. Methods: The Human Oral Microbe Identification Microarray was used to test for the presence of 272 bacterial species in 333 upper digestive tract samples from a Chinese cancer screening cohort. Serum PGI and PGII were determined by ELISA. ESD was determined by chromoendoscopy with biopsy. Results: Lower microbial richness (number of bacterial genera per sample) was significantly associated with lower PGI/II ratio (P 0.034) and the presence of ESD (P 0.018). We conducted principal component (PC) analysis on a b-diversity matrix (pairwise difference in microbiota), and observed significant correlations between PC1, PC3, and PGI/II (P 0.004 and 0.009, respectively), and between PC1 and ESD (P 0.003). Conclusions: Lower microbial richness in upper digestive tract was independently associated with both cancer-predisposing states in the esophagus and stomach (presence of ESD and lower PGI/II). Impact:These novel findings suggest that the upper digestive tractmicrobiotamayplay a role in the etiology of chronic atrophic gastritis and ESD, and therefore in the development of gastric and esophageal cancers. Cancer Epidemiol Biomarkers Prev; 23(5); 735–41. 2014 AACR
-
1 Title: Serum Pepsinogens and risk of gastric and esophageal cancers in the General Population Nutrition Intervention Trial cohort
2016Co-Authors: Jian-song Ren, Philip R Taylor, Farin Kamangar, S M Dawsey, Youlin Qiao, Hao Liang, Bin Liu, Jin-hu Fan, Christian CAbstract:2 Objective: Low serum Pepsinogen I (PGI) and low Pepsinogen I/Pepsinogen II ratio (PGI/II ratio) are markers of gastric fundic atrophy. We aimed to prospectively test the association between serum PGI/II ratio and risks of gastric noncardia adenocarcinoma, gastric cardia adenocarcinoma, and esophageal squamous cell carcinoma (ESCC). Design: Case-cohort study nested in a prospective cohort with over 15 years of follow-up. Setting: Rural region of the People’s Republic of China. Subjects: Men and women aged 40-69 at study baseline. Main outcome measures: Adjusted hazard ratios and 95 % confidence intervals for the association between serum PGI/II ratio and caner risk. Results: Compared to subjects with PGI/II ratio of> 4, those with ≤4 had HRs (95%CIs) of 2.72 (1.77-4.20) and 2.12 (1.42-3.16) for noncardia and cardia gastric adenocarcinomas, respectively. Risk of both cancers was also increased when we used other cut points ranging from 3 to 6, or quartile models, or nonlinear continuous models. Risk of ESCC was marginall
-
association between upper digestive tract microbiota and cancer predisposing states in the esophagus and stomach
Cancer Epidemiology Biomarkers & Prevention, 2014Co-Authors: Mitchell H. Gail, Youlin Qiao, Jin-hu Fan, Jianxin Shi, Bruce J. Paster, Bruce A. Dye, Vanja Klepacceraj, Guoqing Wang, Wenqiang Wei, S M DawseyAbstract:Background: The human upper digestive tract microbial community (microbiota) is not well characterized and few studies have explored how it relates to human health. We examined the relationship between upper digestive tract microbiota and two cancer-predisposing states, serum Pepsinogen I/Pepsinogen II ratio (PGI/II; predictor of gastric cancer risk) and esophageal squamous dysplasia (ESD; the precursor lesion of esophageal squamous cell carcinoma; ESCC) in a cross-sectional design. Methods: The Human Oral Microbe Identification Microarray was used to test for the presence of 272 bacterial species in 333 upper digestive tract samples from a Chinese cancer screening cohort. Serum PGI and PGII were determined by ELISA. ESD was determined by chromoendoscopy with biopsy. Results: Lower microbial richness (number of bacterial genera per sample) was significantly associated with lower PGI/II ratio ( P = 0.034) and the presence of ESD ( P = 0.018). We conducted principal component (PC) analysis on a β-diversity matrix (pairwise difference in microbiota), and observed significant correlations between PC1, PC3, and PGI/II ( P = 0.004 and 0.009, respectively), and between PC1 and ESD ( P = 0.003). Conclusions: Lower microbial richness in upper digestive tract was independently associated with both cancer-predisposing states in the esophagus and stomach (presence of ESD and lower PGI/II). Impact: These novel findings suggest that the upper digestive tract microbiota may play a role in the etiology of chronic atrophic gastritis and ESD, and therefore in the development of gastric and esophageal cancers. Cancer Epidemiol Biomarkers Prev; 23(5); 735–41. ©2014 AACR . This article is featured in Highlights of This Issue, [p. 685][1] [1]: /lookup/volpage/23/685?iss=5
-
serum Pepsinogens and helicobacter pylori in relation to the risk of esophageal squamous cell carcinoma in the alpha tocopherol beta carotene cancer prevention study
Cancer Epidemiology Biomarkers & Prevention, 2010Co-Authors: Michael B Cook, Philip R Taylor, Christian C Abnet, S M Dawsey, Lena Diaw, Martin J Blaser, Guillermo I Perezperez, Demetrius Albanes, Jarmo Virtamo, Farin KamangarAbstract:Background: Helicobacter pylori can induce gastric atrophy in humans, which in turn increases gastric cancer risk. Whether H. pylori and gastric atrophy also affect the risk of esophageal squamous cell carcinoma (ESCC), however, remains unresolved. Methods: We performed a nested case-control study within the prospective Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study to assess these relationships. The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study is composed of 29,133 Finnish male smokers, ages 50 to 69 years, who were recruited during 1985-1988. Using baseline sera, we assessed H. pylori status (via immunoglobulin G antibodies against whole-cell and CagA antigens) and gastric atrophy status [via the biomarkers Pepsinogen I (PGI) and Pepsinogen II (PGII)] in 79 ESCC cases and 94 controls. Logistic regression with adjustment for age, date of blood draw, education, cigarette smoking, alcohol, body mass index, and fruit and vegetable intake was used to estimate odds ratios (OR) and 95% confidence intervals (95% CI). Results: Gastric atrophy (PGI/PGII <4) was associated with ESCC (OR, 4.58; 95% CI, 2.00-10.48). There was no evidence for an association between H. pylori and ESCC (OR, 0.94; 95% CI, 0.40-2.24). Conclusions: These results could be explained by misclassification of H. pylori status due to serologic amnesia, ESCC risk being dependent on the functional consequences or interactions of H. pylori rather than the infection per se, gastric atrophy having a different histogenesis in ESCC without being primarily dependent on H. pylori acquisition, or a lack of statistical power to detect an effect. Impact: Validation of these results may warrant mechanistic studies to determine the route of association between gastric atrophy and ESCC. Cancer Epidemiol Biomarkers Prev; 19(8); 1966–75. ©2010 AACR. This article is featured in Highlights of This Issue, [p. 1887][1] [1]: /lookup/volpage/19/1887
-
serum Pepsinogens and gastrin 17 and gastric and esophageal cancers a long term prospective study
Journal of Clinical Oncology, 2008Co-Authors: Farin Kamangar, Philip R Taylor, Christian C Abnet, S M Dawsey, Youlin QiaoAbstract:4561 Background: Recent studies have suggested that gastric atrophy, as indicated by low serum Pepsinogen I/ Pepsinogen II ratio (PGI/II ratio), is associated with increased risks of esophageal squ...
Farin Kamangar - One of the best experts on this subject based on the ideXlab platform.
-
1 Title: Serum Pepsinogens and risk of gastric and esophageal cancers in the General Population Nutrition Intervention Trial cohort
2016Co-Authors: Jian-song Ren, Philip R Taylor, Farin Kamangar, S M Dawsey, Youlin Qiao, Hao Liang, Bin Liu, Jin-hu Fan, Christian CAbstract:2 Objective: Low serum Pepsinogen I (PGI) and low Pepsinogen I/Pepsinogen II ratio (PGI/II ratio) are markers of gastric fundic atrophy. We aimed to prospectively test the association between serum PGI/II ratio and risks of gastric noncardia adenocarcinoma, gastric cardia adenocarcinoma, and esophageal squamous cell carcinoma (ESCC). Design: Case-cohort study nested in a prospective cohort with over 15 years of follow-up. Setting: Rural region of the People’s Republic of China. Subjects: Men and women aged 40-69 at study baseline. Main outcome measures: Adjusted hazard ratios and 95 % confidence intervals for the association between serum PGI/II ratio and caner risk. Results: Compared to subjects with PGI/II ratio of> 4, those with ≤4 had HRs (95%CIs) of 2.72 (1.77-4.20) and 2.12 (1.42-3.16) for noncardia and cardia gastric adenocarcinomas, respectively. Risk of both cancers was also increased when we used other cut points ranging from 3 to 6, or quartile models, or nonlinear continuous models. Risk of ESCC was marginall
-
AUCs for discrimination of fundic atrophy (dark bar), and nonatrophic pangastritis (dotted bar represents the study population after exclusion of fundic atrophy from reference group, diagonal lined bar represents whole study population).
2013Co-Authors: Dariush Nasrollahzadeh, Farin Kamangar, Christian C Abnet, Karim Aghcheli, Masoud Sotoudeh, Ramin Shakeri, Christina E. Persson, Farhad Islami, Paolo Boffetta, Lars EngstrandAbstract:AUC: Area under curve, PGI: Pepsinogen I, PGII. Pepsinogen II, PGI/PGII ratio: Pepsinogen I/Pepsinogen II ratio, G-17: gastrin-17.
-
Screening characteristics of PGI and PGI/PGII ratio for diagnosis of fundic atrophy and nonatrophic pangastritis.
2013Co-Authors: Dariush Nasrollahzadeh, Farin Kamangar, Christian C Abnet, Karim Aghcheli, Masoud Sotoudeh, Ramin Shakeri, Christina E. Persson, Farhad Islami, Paolo Boffetta, Lars EngstrandAbstract:CI: confidence interval, AUC: area under curve, PPV: positive predictive value, NPV: negative predictive value, PGI: Pepsinogen I, PGII: Pepsinogen II, G-17: gastrin-17.
-
Levels of Pepsinogens, gastrin, and percentage of subjects seropositive for H. pylori, and CagA according to the topography of moderate/marked gastritis and atrophy.
2013Co-Authors: Dariush Nasrollahzadeh, Farin Kamangar, Christian C Abnet, Karim Aghcheli, Masoud Sotoudeh, Ramin Shakeri, Christina E. Persson, Farhad Islami, Paolo Boffetta, Lars EngstrandAbstract:SD: Standard deviation, IQR: interquartile range, PGI: Pepsinogen I, PGII: Pepsinogen II, CagA: cytotoxin-associated gene A, PPI (proton pump inhibitor).*H. pylori status was determined according to the results of histology examination, ELISA IgA/IgG, and Western blot.
-
gastric atrophy and oesophageal squamous cell carcinoma possible interaction with dental health and oral hygiene habit
British Journal of Cancer, 2012Co-Authors: Dariush Nasrollahzadeh, Farin Kamangar, Karim Aghcheli, Farhad Islami, Reza Malekzadeh, M Sotoudeh, Shahin Merat, Christian C AbnetAbstract:Gastric fundal atrophy has been hypothesised to increase the risk of oesophageal squamous cell carcinoma (OSCC), but studies have shown inconsistent results. We measured serum Pepsinogen I (PGI) and Pepsinogen II (PGII) among 293 incident cases and 524 matched neighbourhood controls in a high-risk area of Northern Iran. Conditional logistic regression model was used to estimate odds ratios (ORs) and their 95% confidence intervals (CIs). After controlling for age, sex, residence area and other potential confounders, gastric atrophy (defined by a validated criterion, PGI <55 μg dl−1) was associated with a two-fold increased risk (OR=2.01, 95% CI: 1.18, 3.45) of OSCC in the absence of nonatrophic pangastritis (defined as PGII <11.8 μg dl−1). Stratification by PGII decreased the misclassification errors due to cancer-induced gastritis. Presence of both poor dental health, indicated by higher than median sum of decayed, missing, and filled teeth (DMFT score), and gastric atrophy further increased the risk of OSCC (OR=4.15, 95% CI: 2.04, 8.42) with relative excess risk due to interaction (RERI) of 1.47 (95% CI: −1.15, 4.1). Coexistence of poor oral hygiene habit with gastric atrophy elevated OSCC risk eight times (OR=8.65, 95% CI: 3.65, 20.46) and the additive interaction index was marginally statistically significant (RERI=4.34, 95% CI: −1.07, 9.76). Gastric atrophy is a risk factor for OSCC, and poor dental health and oral hygiene habit may act synergistically in increasing the risk.