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sT1647

Association of Helicobacter pylori Gastritis with Anemia: A Nation-Wide Studyof 77,000 AdultsRobert M. Genta

Purpose: Several reports have shown an association between H. pylori gastritis and anemia.However, it remains unclear whether the prevalence of H. pylori is greater in patients whoundergo EGD for the workup of anemia than in patients investigated for other signs orsymptoms. In this study we used a nation-wide sample of patients who underwent EGDwith gastric biopsies to assess the relationship between clinical indications for EGD, includinganemia, andH. pylori infection.Methods:We analyzed electronic data fromCaris Diagnostics,a specialized gastrointestinal pathology group receiving specimens from community-basedendoscopy centers in 40 states. The database includes demographic and clinical information,a summary of the endoscopy report, site of origin, and histopathologic report for eachbiopsy. We extracted data from all patients who underwent an EGD with gastric biopsiesfrom 4/01/07 to 3/31/08. Statistical calculations were performed using SigmaStat 3.5; oddratios were calculated using Hutchon's online calculator. A p value < 0.05 was consideredsignificant. Results: Gastric biopsies were available from 78,899 unique patients (65.6 %women; median age 52 years, range 0-92). Since only 16 (1.1%) of 1,408 children (age 18or younger) had anemia as an indication for EGD, children were excluded from the analysis.After excluding 268 patients with gastric malignancies, we analyzed data from 77,223 adults.Histologically, 21.5% had a normal gastric mucosa; 39.5% had various degrees of chronicinactive gastritis; 12.1% had H. pylori gastritis; and 7.4% had atrophy/intestinal metaplasia.Patients undergoing EGD for dyspepsia (42.5%) or GERD (37.6%) had a prevalence of thesehistologic diagnoses similar to those of all adults. In contrast, when compared to the 71,218patients who underwent EGD for other indications, the 6,005 patients undergoing EGD foranemia (7.8% of all adults) had a significantly greater prevalence of H. pylori gastritis (16.6%,OR 1.49, 95% CI 1.39-1.60; p<0.01) and of atrophy/metaplasia (10.1%, OR 1.44, 95% CI1.32-1.57; p<0.01), while they were less likely to have a normal gastric mucosa (15.9%,OR 0.67, 95% CI 0.63-0.72; p<0.01). Conclusion: Adults undergoing EGD for the investi-gation of anemiawere approximately 50%more likely to have H. pylori infection ormetaplasticatrophy than patients with other EGD indications. These data provide further support fora possible role for H. pylori in the pathogenesis of anemia, either directly (through gastricmucosal inflammation) or indirectly (through the induction of metaplastic atrophy).

T1648

Ethnic Differences in the Acquisition of Helicobacter pylori Infection AmongChildren in North VietnamVanBang Nguyen, Nguyen GIA Khanh, Phung Dac Cam, Hoda M. Malaty

Background: The epidemiology of H. pylori (Hp) infection and risk factors associated withits transmission vary between developed and developing countries and within the samecountry. Hypothesis: Ethnicity has been documented to play a significant role in the transmis-sion of Hp infection. Vietnam is a developing country with a population of 85 millions and54 different ethnic groups. Aim: To examine the prevalence and associated risk factors, andpossible mode of transmission of Hp infection among five ethnic groups in Vietnam. Popula-tion and Methods: A cross-sectional sero-epidemiologic study was conducted in householdsresiding in a mountainous village (Ban Qua) of a northern border province (Laocai). Fiveethnic groups were included in the current study; H'mông, Tay, Dao and Giay (minorityethnic groups) and Kinh (majority ethnic group). Demographic information, living condi-tions, number of siblings in the family, breast feeding practices and family history of uppergastrointestinal diseases were collected by using a standardized questionnaire. Enzyme-linked immunosorbent assay (ELISA) was used for the detection of anti-H. pylori-IgG. Results:The studied population consisted of 245 households with a total number of 408 childrenbetween the ages of 6 months to 18 years. The overall prevalence of Hp infection amongchildren was 26.7%; increased with age (≤3 years: 9.2%, 3-6 years: 21.5%, 6-10 years:26.2%, 10-18 years: 36.9%, p<0.02) but without significant difference between boys andgirls 27.7% Vs. 25.7%, respectively, (p>0.0). Ethnicity revealed a significant effect on Hpprevalence; 16.1% in H'mông, 16.7% in Tay, 20.3% in Dao, 38.5% in Giay, and 41.0% inKinh (p<0.001). Breastfeeding more than 6 months was negatively and independently associ-ated with H. pylori seropositivity (OR 0.5, 95% CI=0.3-0.9). Number of off-spring werepositively associated with H. pylori infection (OR=1.1-2.6, 95% CI= 2.9-1.8). After applyinglogistic regression analysis, additional risk factors emerged for the acquisition of HP infectionamong the studied children, e.g. positive HP status among sibling, family history of upperGI disorders, and infected parents with HP. Conclusions: H. pylori prevalence in minorityethnic groups was lower than in the majority ethnic group. Of interest, the risk factors forHP acquisition did not differ between the five studied ethnic groups. Understanding theepidemiology of H. pylori infection in childhood requires better understanding of the interac-tions between environment, ethnic groups, and socioeconomic conditions.

T1649

Changes in Gastric Acidity After Eradication Therapy for Helicobacter pylori inPatients Under 40 Years of Age: When Is the “Point of No Return” Reached?Tomohiko Shimatani, Ayumi Furukawa, Seiko Hirokawa, Yumiko Tawara, Kazuko Hamai,Mutsuko Matsumoto, Susumu Tazuma, Masaki Inoue

BACKGROUND: Helicobacter pylori (H. pylori) infection affects gastric acidity and can bemore or less recovered by eradication therapy. However, it is unknown at what age the“point of no return” is reached. AIMS: To investigate whether gastric acidity normalizesafter eradication therapy for H. pylori in patients under 40 years of age. METHODS: 42 H.pylori-positive patients, aged between 20 and 39 years, and 45 age- and sex-matched H.pylori-negative subjects (N) were enrolled. 1) All patients underwent endoscopy. Four speci-mens were biopsied, two from the antrum and two from the upper corpus along the greatercurvature. 2) H. pylori status was evaluated by a histologic examination, a rapid urease testand the serum H. pylori-IgG antibodies. 3) The degree of mononuclear cell infiltration withinthe lamina propria (inflammation) and of glandular atrophy were scored from 0 to 3 according

A-550AGA Abstracts

to the updated Sydney system. If the score in each specimen was 2 or 3, they were consideredto be positive. 4) Serum pepsinogen (PG) I and II concentrations were determined. 5)Intragastric pH was measured for 24-h. 6) All H. pylori-positive patients consented toeradication therapy. At 6 to 8 months after successful eradication as determined by a 13C-urea breath test, intragastric pH was measured again. Serum PGs were also measured.RESULTS: In the 22 H. pylori-positive pangastritis, median intragastric pH value (medianpH) and % time with intragastric pH > 4 (% pH > 4) for 24-h were significantly higher[median 3.4 (25th-75th percentile 3.0-3.7) and 39% (35-47%)] than those in N [2.1 (1.9-2.4) and 16% (11-26%)] and in the 20 H. pylori-positive antrum-predominant gastritis [2.2(1.8-2.8) and 19% (14-28%)] (p < .0001, respectively). After eradication for H. pylori,these two parameters significantly decreased [2.2 (1.8-2.4) and 24% (16-29%), p < .0001,respectively] and reached the same ranges as those in N. 9 patients were compatible withthe serological atrophy-positive criterion (PG I≦ 70 ng/mL and PG I/II ratio≦ 3.0), althoughnone was histologically diagnosed with atrophic gastritis. Median pH and % pH > 4 weresignificantly higher in atrophic gastritis [3.4 (2.8-3.8) and 44% (33-47%)] than those in N(p < .0001, respectively) and in non-atrophic gastritis [2.7 (2.1-3.1) and 28% (16-37%), p< .05, respectively]. After successful eradication, these parameters also significantly decreased[2.2 (1.8-2.3), p < .01 and 26% (15-30%), p < .05] and reached the same ranges as thosein N. CONCLUSIONS: In patients under 40 years of age, even in pangastritis and atrophicgastritis, gastric acidity can be completely normalized by eradication therapy for H. pylori.

T1650

CagA-Positive Strains of H. pylori Cross React with Trophoblast Cells: A Rolefor Pre-Eclampsia and Poliabortivity?Francesco Franceschi, Nicoletta Di Simone, Giovanni Gigante, Davide Roccarina, BiancaGiupponi, Veronica Ojetti, Guido De Marco, Federico Barbaro, Roberta Castellani, MariaClara D'Alessio, Fiorella Di Nicuolo, Silvia D'Ippolito, Chiara Tersigni, GiovanniGasbarrini, Antonio Gasbarrini, Alessandro Caruso, Nicolò Gentiloni Silveri

Background: The role of bacterial and viral infections in trophoblast diseases, such as pre-eclampsia and poliabortivity, has been extensively studied in the past few years. Interestingly,while trophoblast cells show an endothelial phenotypic profile, a study from our group hasshown that antibodies anti-CagA cross-react with endothelial cells, possibly playing a rolein some vascular diseases. Based on this finding, we have hypothesized that CagA-positivestrains of H. pylori may also recognize antigens of trophoblast cells, thus impairing theirinvasion capability. To clarify this point we have evaluated In Vitro: 1. whether anti-CagAantibodies may recognize antigens of trophoblast cells; 2. whether anti-CagA antibodies mayaffect invasiveness of isolated trophoblast cells; 3. whether antibodies anti-CagA may modu-late Matrix Metalloprotease-2 (MMP-2) protein activity. Materials and Methods: Placentasamples were obtained from healthy women. Trophoblast cells were cultured for 72 hoursin a medium containing increasing concentration of polyclonal anti-CagA antibodies (from6 to 200 μg/ml). Binding of anti-CagA antibodies to trophoblast cells was verified throughflow cytofluorimetry and immunoflurescence, while the invasive potential of these cells wasassessed by using a membrane invasion culture system. MMP-2 activity was evaluated bygelatin zimography. Results: We observed that anti-CagA antibodies recognized antigens oftrophoblast cells of all samples, showing a dose-dependent binding up to the highestconcentration of 200 μg/ml. This data has also been confirmed by immunofluorescence.Incubation of trophoblast cells with increasing doses of anti-CagA antibodies significantlyreduced their invasiveness. Furthermore these data were confirmed by a significant reductionof MMP-2 protein activity. Conclusions: This preliminary study reports, for the first time,that anti-CagA antibodies are able to recognize antigens expressed on the surface of tropho-blast cells, and to reduce their invasiveness ability. The inhibitory effect of anti-CagA antibod-ies on trophoblast cells is directly related to the concentration of the same antibodies. Thesedata give biological plausibility to the theory that CagA-positive strains of H. pylori mayplay a role in trophoblast-related diseases, such as pre-eclampsia and poliabortivity. Furtherstudies are now needed in order to identify the cross-reactive antigens responsible forthis phenomenon.

T1651

The Natural History of Gastric Ulcer: A Twenty-Four Years Clinical-Endoscopical Follow-UpFrancesco Di Mario, Loredana Guida, Margherita Curlo, Andrea Iori, Ester Morana, LucasG. Cavallaro, Nadia Dal Bò, Carmelo Scarpignato, Giulia Martina Cavestro, AlbertoPilotto, Angelo Franzè, Massimo Rugge

Background: the natural history of peptic ulcer has been completely changed after thediscovery of the role of the Helicobacter pylori in 1980's. The majority of studies on thistopic, however, are related to duodenal ulcer and very few data about gastric ulcer includedfollow-up over two years. Aim: Aim of our study, therefore, was twofold: 1. To establishthe ethiologic role of Helicobacter pylori infection in a large cohort of gastric ulcer patients;2. To evaluate the impact of H. pylori eradication on the relapse rate in such patients lastinga twenty-four years follow-up. Methods: Four hundred forty-seven consecutive patients (F189, M 258, mean age 56 years, range 18-84 years) with endoscopically proved gastric ulcerwere enrolled in the study from 1976 to 2000. The mean follow-up was 38 months, range3-256. After baseline endoscopy with appropriated biopsies to assess the benignity of thelesions, a clinical assessment was performed every six months and a new endoscopy every twoyears. Each episode of recurrence of symptoms lasting more than five days was investigated bymeans of an addictional endoscopy. The study was intended as a monocenter study, beingall the patients followed-up and endoscopized by the same team of four physicians. Results:Overall, 44.7% of the patients resulted H. pylori positive (based on gastric mucosa histology).According with H. pylori status the number of relapses lasting the follow-up was as follows:Hp positive pts: < 1 relapse: 39%, 2-3 relapses: 20%, > 4 relapses: 41%; Hp negative pts:<1 relapse: 62%, 2-3 relapses: 28%, > 4 relapses: 10%. In the “pre-eradication” period(1976-1988) 85 relapses of gastric ulcers were observed against 15 in the “post-eradication”period (1988-2000). Conclusions: H. pylori infection has been detected in less than 50% ofgastric ulcer patients. In H. pylori infected gastric ulcer patients the number of relapses