Conclusions:Both H. pylori infection and NSAID use independently andsignificantly increase the relative risk of peptic ulcer.H. pylori infectionfurther increases the risk of ulcer over that seen with NSAIDs alone. Thus,there is a synergism between these two risk factors on peptic ulceration.

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Helicobacter pylori eradication with tetracycline, furazolidone andbismuth (TFB), and rate of reinfection one year after successfultreatmentD de Idiaquez, MD, C Seminario, MD, J Huerta Mercado, MD, JCabello, MD, J Cok, MD, A Bussalleu, MD, FACG. Peruvian UniversityCayetano Heredia, Lima, Peru.

H. pylori (HP) is a prevalent infection in Peru. High rates of resistanceagainst some antibiotics as well as elevated costs affect the effectiveness ofsome therapies.Aim: To assess the effectiveness of the combination of tetracycline, fura-zolidone and bismuth in eradicating HP; changes in histologic pattern; andthe reinfection rate one year after HP eradication.Methods: Patients with HP infection, found in antral biopsies with HEstaining, were included. They received for ten days tetracycline 500 mg qid,furazolidone 100 mg qid, and colloidal bismuth subcitrate 120 mg qid.Patients were instructed to come back 8 weeks after starting therapy, wherefour antral biopsies were taken. Biopsies done before and after treatmentwere evaluated for: presence and density of HP; depth and grade of chronicgastritis, presence and grade of inflammatory activity, glandular atrophy,grade and extent of mucinous damage, presence of intestinal metaplasia,and presence of lymphoid follicles. Patients with HP negative control wereevaluated one year later with biopsies to determine reinfection.Results:59 patients (30 men and 29 women) completed per protocol, agerange 14–73, HP eradication was achieved in 54 (91.5%). Control biopsiesof these 54 patients showed improvement in all the histologic parameters(p,0.001) except in glandular atrophy and intestinal metaplasia. Thirty of54 patients negative for HP were evaluated a year later for reinfection.Three (10%) were again positive for HP.Conclusions:TFB scheme is effective in HP eradication. This is followedby an improvement in several histologic parameters. Although 10% be-come reinfected we consider this scheme is cost-effective for HP infectionin low income populations with high HP infection prevalence.

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Hp eradication rates and symptoms in patients with proven pepticulcersChin Hur, MD, Pierre F. Michetti, MD, Ciavan Kelly, MD. Beth IsraelDeaconess Medical Center/Harvard Medical School, Boston, MA, USA.

Purpose: A large amount of published data unequivocally supports thepractice of Helicobacter pylori (Hp) eradication in patients with pepticulcer disease (PUD). The aim of this study was to determine what per-centage of patients with endoscopically diagnosed PUD were treated anderadicated and its effect on symptoms.Methods: Patients with PUD were identified from a review of our insti-tution’s endoscopy records from 1995 to 1998. Out of the patients identi-fied, those who had documented Hp infection by either pathology orserology were eligible for our study. Study participation involved com-pleting a questionnaire and then providing a stool sample. We used theMeridian Diagnostics Hp stool antigen test (EIA) to check for currentinfection. Out of 174 patients contacted, 53 completed the study (30.5%).Results:

● Of the 53 patient stools tested for active Hp infection, 3/53 (5.7%) werepositive. All three patients who were positive reported that they hadcompleted eradication therapy.

● 46 out of 53 (86.8%) recalled having been treated for their Hp infectionand 45 out of the 46 (97.8%) reported that they finished their regimen.

● 38 out of 53 (71.4%) reported digestive symptoms with their original

ulcer. 26 out of 38 (68.4%) no longer have symptoms after eradicationwhile 11/37* (29.7%) continued to have symptoms after eradication atthe time of survey.*(One of the symptomatic patients was not eradicated.)

Conclusions:A substantial percentage of patients who had symptoms withtheir ulcer and infection continue to have these symptoms even aftersuccessful eradication.

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The intestinal metaplasia of the gastric cardia is associated withHelicobacter pyloriinfectionSeong Gook Jeon, Yi Kyung Chun. Samsung Cheil Hospital,Sungkyunkwan University School of Medicine, Seoul, Korea.

Purpose: Whether cardia intestinal metaplasia (IM) is associated withgastroesophageal reflux disease (GERD) orHelicobacter pylori(H. pylori)infection is unknown. The aim of the present study was to investigate therole of GERD andH. pylori infection in the development of cardia IM.Methods: Thirty-seven consecutive patients with reflux esophagitis onEGD were studied. Age and sex matched, 32 asymptomatic subjects wereused as a control group. Exclusion criteria included the use of antibioticswithin 30 days before EGD, prior gastric or esophageal surgery, currentpeptic ulcer disease or gastric cancer and previousH. pylori eradication.Two biopsy specimens were obtained from antrum, body, fundus andcardia, respectively. All biopsy specimens were stained with H&E, alcian-blue and Giemsa. The severity of gastritis was graded according to theupdated Sydney system.Results: Carditis in controls was more severe than that in patients withreflux esophagitis. The prevalence rate ofH. pylori increased with greaterdegree of carditis in each groups (p,0.05). The prevalence of cardia IMwas not significantly different between patients with reflux esophagitis(24.3%) and controls (46.7%). ButH. pylori infection was more commonin subjects with cardia IM compared to subjects without cardia IM in eachgroups (p,0.05).Conclusions: Cardia IM is associated withH. pylori infection, but notGERD.

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Does a Cox-2 inhibitor, rofecoxib have low potential for causingacute gastric lesion: “A double blind, randomized, placebocontrolled trial”Kapioroglu1 S, Bafu1 A, Kayrier1 K, Aydun2 F, Ozoran3 Y. Karadeniz(Black Sea) Technical University, School of Medicine, Department ofInternal Medicine, Section of Gastroenterology1, Department ofMicrobiology2, and Pathology3, Trabzon, Turkey.

Purpose: In this study it was aimed to examine the effect of rofecoxib, aselective inhibitor of COX-2 enzyme, to the acute gastric mucosal lesionand to correlate its effect with aspirin.Methods: This study was planned as double blind, randomized and placebocontrolled. Mean age of voluntary persons (n:26) was 4762.98 divided intothree groups. Patients were excluded if they had active duodenal, gastric oroesophageal ulcers or oesophagitis at baseline endoscopy. Volunteers weregiven randomized placebo (n:10), aspirin (n:10) (500 mg aspirin-Bayer,Germany), and rofecoxib (n:16) (VIOXX 50 mg MSD, USA) with 50 mlof water after 12 hours fasting period at 08.00 a.m. Three hours after eachtherapy, gastroduodenoscopy was performed to the volunteers. Mucosa ofduodenum and stomach was screened by endoscopy. Biopsies were takento determine the presence of histopathology and H. pylori. Treatmentgroups were similar at baseline with respect to age, sex, H. pylori status,alcohol or smoking use.Results: Endoscopic scores of groups were: 0.6060.28 in placebo,3.3060.25 in aspirin, and 0.5960.25 in rofecoxib. Acute gastric lesionscore in rofecoxib group was similar with placebo group. Lesion scoreswere found significantly high in aspirin group when compared with placebo

2454 Abstracts AJG – Vol. 95, No. 9, 2000