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Plasma Levels of Insulinotropic and Digestive Hormones Predict the Risk of Colonic Adenomas [Meeting Abstract]
Wolff, Martin J; Joseph, Neal; Huie, Maryann L; Quijano, Sergio; Muakkassa, Nora; Martiniuk, Frank; Perez-Perez, Guillermo I; Francois, Fritz
ISI:000275277203085
ISSN: 0016-5085
CID: 1716332
Relation of atrophic gastritis with Helicobacter pylori-CagA(+) and interleukin-1 gene polymorphisms
Sierra, Rafaela; Une, Clas; Ramirez, Vanessa; Alpizar-Alpizar, Warner; Gonzalez, Maria-I; Ramirez, Jose-A; De Mascarel, Antoine; Cuenca, Patricia; Perez-Perez, Guillermo; Megraud, Francis
AIM: To determine the association of Helicobacter pylori (H pylori) CagA(+) infection and pro-inflammatory polymorphisms of the genes interleukin (IL)-1RN and IL-1B with the risk of gastric atrophy and peptic ulcers in a dyspeptic population in Costa Rica, a country with high incidence and mortality of gastric cancer. METHODS: Seven biopsy specimens, a fasting blood sample and a questionnaire concerning nutritional and sociodemographic factors were obtained from 501 consecutive patients who had undergone endoscopy for dyspeptic symptoms. A histopathological diagnosis was made. Pepsinogen concentrations were analyzed by enzyme linked immunosorbent assay (ELISA). Infection with H pylori CagA(+) was determined by serology and polymerase chain reaction (PCR). IL-1B and IL-1RN polymorphisms genotyping was performed by PCR-restriction fragment length polymorphism (PCR-RFLP) and PCR respectively. RESULTS: In this dyspeptic population, 86% were H pylori positive and of these, 67.8% were positive for CagA. Atrophic antral gastritis (AAG) was associated with CagA(+) status [odd ratio (OR) = 4.1; P < 0.000] and fruit consumption (OR = 0.3; P < 0.00). Atrophic body gastritis (ABG) was associated with pepsinogen PGI/PGII < 3.4 (OR = 4.9; P < 0.04) and alcohol consumption (OR = 7.3; P < 0.02). Duodenal ulcer was associated with CagA(+) (OR = 2.9; P < 0.04) and smoking (OR = 2.4; P < 0.04). PGI < 60 microg/L as well as PGI/PGII < 3.4 were associated with CagA(+). CONCLUSION: In a dyspeptic population in Costa Rica, H pylori CagA(+) is not associated with ABG, but it is a risk factor for AAG. The pro-inflammatory cytokine polymorphisms IL-1B + 3945 and IL-1RN are not associated with the atrophic lesions of this dyspeptic population
PMCID:2773333
PMID: 19030199
ISSN: 1007-9327
CID: 102590
Association of Helicobacter pylori infection and diet on the risk of gastric cancer: a case-control study in Hawaii
Epplein, Meira; Nomura, Abraham M Y; Hankin, Jean H; Blaser, Martin J; Perez-Perez, Guillermo; Stemmermann, Grant N; Wilkens, Lynne R; Kolonel, Laurence N
OBJECTIVE: The risk factors most strongly associated with gastric cancer are the gastric bacteria Helicobacter pylori and diet. Utilizing data from a case-control study among residents in Hawaii, we examined the association of diet, presence of H. pylori, and non-cardia gastric cancer risk. METHODS: Serum taken at diagnosis for cases (n = 212) and at interview for controls (n = 336) was assayed for IgG antibodies to H. pylori group antigens and to a recombinant fragment of the cytotoxin-associated antigen A (CagA) protein, and subjects completed food frequency questionnaires. Risk measures were calculated using logistic regression. The likelihood ratio test was used to assess interactions. RESULTS: Inverse associations were found between gastric cancer risk and increasing intake of several micronutrients and vegetables among all individuals. For H. pylori/CagA-positive subjects, significant trends were present for total, green, and yellow vegetables, while a significant trend was present only for yellow vegetables among H. pylori/CagA-negative individuals. For intestinal gastric cancer, there was a suggestion that intake of vegetables, especially cruciferous vegetables, had a stronger protective effect for the H. pylori/CagA-positive group. CONCLUSIONS: Diet may play a greater role in the etiology of non-cardia gastric cancer among individuals with evidence of H. pylori infection than among those without
PMCID:2799111
PMID: 18369531
ISSN: 0957-5243
CID: 79187
Evaluation of serum pepsinogen I and II levels, gastrin-17 and H. pylori antibodies in patients with dyspepsia [Meeting Abstract]
Yilmaz, O; Demiray, E; Soyturk, M; Perez, GIP; Sagol, O; Bekmen, N; Simsek, I; Akpinar, H
ISI:000258404600183
ISSN: 1083-4389
CID: 86819
Prevalence of H. pylori in Georgian pediatric patients with peptic ulcer diseases [Meeting Abstract]
Buadze, M; Olivares, A; Kutubidze, T; Labauri, L; Chavchanidze, D; Lobzhanidze, G; Perez-Perez, GI
ISI:000258404600165
ISSN: 1083-4389
CID: 86817
The effect of H. pylori eradication on serum pepsinogen I and II levels, gastrin-17, and H. pylori antibodies in patients with dyspepsia [Meeting Abstract]
Yilmaz, O; Demiray, E; Soyturk, M; Perez, GIP; Sarioglu, S; Bekmen, N; Simsek, I; Akpinar, H
ISI:000258404600181
ISSN: 1083-4389
CID: 86818
mRNA levels of TLR4 and TLR5 are independent of H pylori
Garza-Gonzalez, Elvira; Bocanegra-Garcia, Virgilio; Bosques-Padilla, Francisco-Javier; Flores-Gutierrez, Juan-Pablo; Moreno, Francisco; Perez-Perez, Guillermo-Ignacio
AIM: To determine if the presence H pylori or its virulence affect toll-like receptor 4 (TLR4) and TLR5 mRNA expression levels. METHODS: For the in vivo assays, gastric biopsies were obtained from 40 patients and H pylori status was determined. For the in vitro assays, human gastric adenocarcinoma mucosal cells (AGS) were cultured in the presence or absence of twelve selected H pylori strains. H pylori strains isolated from culture-positive patients and selected strains were genotyped for cagA and vacA. The cDNA was obtained from mRNA extracted from biopsies and from infected AGS cells. TLR4 and TLR5 mRNA levels were examined by real-time PCR. RESULTS: The presence of H pylori did not affect the mRNA levels of TLR4 or TLR5 in gastric biopsies. The mRNA levels of both receptors were not influenced by the vacA status (P > 0.05 for both receptors) and there were no differences in TLR4 or TLR5 mRNA levels among the different clinical presentations/histological findings (P > 0.05). In the in vitro assay, the mRNA levels of TLR4 or TLR5 in AGS cells were not influenced by the vacAs1 status or the clinical condition associated with the strains (P > 0.05 for both TLR4 and TLR5). CONCLUSION: The results of this study show that the mRNA levels of TLR4 and TLR5 in gastric cells, both in vivo and in vitro, are independent of H pylori colonization and suggest that vacA may not be a significant player in the first step of innate immune recognition mediated by TLR4 or TLR5
PMCID:2744061
PMID: 18785283
ISSN: 1007-9327
CID: 102589
The effect of laparoscopic gastric banding surgeryon plasma levels of appetite-control, insulinotropic, and digestive hormones (Obesity Surgery DOI: 10.1007/s11695-008-9454-6)
Shak, J R; Roper, J; Perez-Perez, G I; Tseng, C -H; Francois, F; Gamagaris, Z; Patterson, C; Weinshel, E; Fielding, G A; Ren, C; Blaser, M J
EMBASE:50180205
ISSN: 0960-8923
CID: 4024662
The Effect of Laparoscopic Gastric Banding Surgery on Plasma Levels of Appetite-Control, Insulinotropic, and Digestive Hormones
Shak, Joshua R; Roper, Jatin; Perez-Perez, Guillermo I; Tseng, Chi-hong; Francois, Fritz; Gamagaris, Zoi; Patterson, Carlie; Weinshel, Elizabeth; Fielding, George A; Ren, Christine; Blaser, Martin J
BACKGROUND: We hypothesized that laparoscopic adjustable gastric banding (LAGB) reduces weight and modulates ghrelin production, but largely spares gastrointestinal endocrine function. To examine this hypothesis, we determined plasma concentrations of appetite-control, insulinotropic, and digestive hormones in relation to LAGB. METHODS: Twenty-four patients undergoing LAGB were prospectively enrolled. Body mass index (BMI) was measured and blood samples obtained at baseline and 6 and 12 months post-surgery. Plasma concentrations of leptin, acylated and total ghrelin, pancreatic polypeptide (PP), insulin, glucose-dependent insulinotropic peptide (GIP), active glucagon-like peptide-1 (GLP-1), gastrin, and pepsinogens I and II were measured using enzyme-linked immunoassays. RESULTS: Median percent excess weight loss (%EWL) over 12 months was 45.7% with median BMI decreasing from 43.2 at baseline to 33.8 at 12 months post-surgery (p < 0.001). Median leptin levels decreased from 19.7 ng/ml at baseline to 6.9 ng/ml at 12 months post-surgery (p < 0.001). In contrast, plasma levels of acylated and total ghrelin, PP, insulin, GIP, GLP-1, gastrin, and pepsinogen I did not change in relation to surgery (p > 0.05). Pepsinogen II levels were significantly lower 6 months after LAGB but returned to baseline levels by 12 months. CONCLUSIONS: LAGB yielded substantial %EWL and a proportional decrease in plasma leptin. Our results support the hypothesis that LAGB works in part by suppressing the rise in ghrelin that normally accompanies weight loss. Unchanged concentrations of insulinotropic and digestive hormones suggest that gastrointestinal endocrine function is largely maintained in the long term
PMCID:3743550
PMID: 18408980
ISSN: 0960-8923
CID: 78623
Leptin and ghrelin in relation to Helicobacter pylori status in adult males
Roper, Jatin; Francois, Fritz; Shue, Peter L; Mourad, Michelle S; Pei, Zhiheng; Olivares de Perez, Asalia Z; Perez-Perez, Guillermo I; Tseng, Chi-Hong; Blaser, Martin J
CONTEXT: Leptin and ghrelin, hormones involved in human energy homeostasis, are both produced in the stomach. OBJECTIVE: We sought to determine whether the presence of Helicobacter pylori affects gastric and systemic levels of leptin and ghrelin. DESIGN, SETTING, AND PATIENTS: We consecutively enrolled 256 patients referred for upper endoscopy at a Veterans Affairs outpatient endoscopy center. OUTCOMES: We obtained fasting serum, fundic and antral biopsies, and gastric juice. Based on histological, biochemical, and serological assays, patients were categorized as H. pylori+ or H. pylori-. Leptin and total ghrelin levels in serum, gastric biopsies, and gastric juice were determined by specific ELISAs. RESULTS: Of the 256 subjects, 120 were H. pylori+ and 96 were H. pylori-; 40 patients of indeterminate status were excluded. Serum and fundic leptin levels correlated with body mass index in the H. pylori+ (r = 0.35; P < 0.0001 and r = 0.35; P < 0.0001, respectively) and H. pylori- (r = 0.65; P < 0.0001 and r = 0.41; P < 0.0001, respectively) groups, but H. pylori+ subjects had significantly lower serum leptin levels [median 2.2 ng/ml (interquartile range 0.9-4.6) vs. 4.0 ng/ml (1.7-7.2); P = 0.0003]. Serum ghrelin levels were similar in the H. pylori+ and H. pylori- groups [median 1651 pg/ml (interquartile range 845-2247) vs. 1629 pg/ml (992-2886); P = 0.23]. H. pylori status did not significantly affect gastric biopsy leptin and ghrelin levels. Ghrelin levels in gastric juice varied over 4 log(10) (<80-776,000 pg/ml) and correlated with gastric juice pH in the H. pylori+ group (r = 0.68; P < 0.0001). CONCLUSIONS: These findings provide evidence that H. pylori status affects leptin and ghrelin homeostasis, presumably via intragastric interactions.
PMCID:2435636
PMID: 18397989
ISSN: 0021-972x
CID: 159212