A1278 AGA ABSTRACTS

5838

PHARMACOLOGIC CONCENTRATIONS OF VITAMIN C IN­HIBIT THE GROWTH OF HEUCOBACTER PYLORI IN VITRO.Anna U. Morgan, Mathew J. Domek, Univ High Sch, Irvine, CA; CA StateUniv, Long Beach, CA.

Research studies have demonstrated decreased concentrations of ascorbicacid in gastric juice of patients infected with Helicobacterpylori. In initialstudies of physiologic concentrations of ascorbic acid, we found thatvitamin C modestly decreased growth of H. pylori in vitro. The purpose ofthis study was to determine the effect of pharmacologic concentrations ofvitamin C on growth of H. pylori in vitro. Pharmacologic concentrations ofvitamin C are readily available from fresh fruits and from various vitaminpreparations. METHODS: H. pylori were grown on 1.5% a~ar (w/v) platesprepared with 2.5% Brucella broth (w/v) and 10% fetal bovine serum (v/v)in the absence (control) and presence of varying concentrations from 50p,g/mL to 5000 p,g/mL of vitamin C. ~ree types of vitamin C were te~ted:

I) vitamin C crystals, 2) Ester-C (calcium ascorbate) and 3) orange JUIceconcentrate. The plates were inoculated with 100 p,L of a suspension of H.pylori in PBS containing approximately 100 cfu per plate. Plates wereincubated at 37°C in 5% carbon dioxide. After four days the number ofcolonies of H. pylori on each plate was counted. RESULTS: At a concen­tration of 5000 p,g/mL, all three forms of vitamin C inhibited the growthof H. pylori by 99%. However, at low vitamin C concentrations (50 p,g/mL- 150 p,g/mL) the orange juice completely inhibited the growth of H. pyloriwhile the other two form of vitamin C only partially inhibited growth (25%- 50% inhibition). CONCLUSIONS: At high concentrations (5000 p,g/p,L),all three types of vitamin C inhibit the growth of H. pylo~i in vitro by I?orethan 99%. However, at lower, but equivalent, concentrations of vitamm C.orange juice is approximately 100-fold more potent than the other forms ofvitamin C in inhibiting growth of H. pylori in vitro.Fu~er studies need tobe conducted to determine which component of orange JUIce IS tOXIC to H.pylori in vitro, and whether orange juice is bactericidal to H. pylori in vivo.

5839DOES HELICOBACTER PYLORI EFFECT GASTRIC MUCIN EX­PRESSION? RELATIONSHIP BETWEEN GASTRIC MUCIN EX­PRESSION AND H. PYLORI COLONIZATION.Sara Morgenstern, Rivka Koren, Steven F. Moss, Gerald Fraser, Eli Okon,Yaron Niv, Dept of Pathology, Beilinson Campus, Rabin Med Ct:,. Tel­Aviv Univ, Petach-Tikva, Israel; Dept of Gastroenterology, BeilinsonCampus, Rabin Med Ctr, Tel-Aviv Univ, Petach-Tikva, Israel; Gastroen­terology Div, St-Luke's-Roosevelt Hosp, Columbia Univ, New York, NY.

Introduction: Helicobacter pylori colonizes the gastric mucous gel layer,the surface epithelium and glands. It has been shown that H. pyloriinfection causes aberrant expression of gastric mucins, MUC 5 and MUC6. Aim: To determine the normal distribution of MUC 5 and MUC 6 in thestomach and to investigate changes in this pattern in the presence of H.pylori and after successful eradi~ation. Methods: S'astric antrum. biopsyspecimens were examined by immunohistochemistry for mucm gene(MUC 5 and MUC 6) expression. Polyclonal antibodies were used to detectamino-acid tandem repeats of each protein. A scoring system (0-3), wasused to assess staining intensity at 4 sites: lumen, foveola, mucous neckcells and glands. H. pylori status was determined by histology and rapidurease test, and considered positive or negative when both tests werepositive or negative, respectively. 49 patients positive for H. pylori, in .36of whom successful eradication was performed, and 11 H. pylon negativepatients were studied. Results: There was a gradient of MUC 5 expression,higher to lower. from the surface to the glands, which ~as more pro­nounced before eradication. Increased MUC 5 synthesis m the mucousneck cells and in the glands was found after H. pylori eradication (p =0.016). MUC 6 was synthesized in the glands more than in the mucousneck cells or foveola. MUC 6 was also secreted into the lumen andprobably comprised the superficial part of the u~stirred mucous layer.Conclusion: H. pylori may change mucous synthesis and secretion m thestomach. This phenomenon may facilitate H. pylori colonization.

5840GASTRIC CORPUS MUCIN EXPRESSION AFTER PARTIALGASTRECTOMY, IN RELATION TO COLONIZATION WITHHELICOBACTER PYLORI.Sara Morgenstern, Rivka Koren, Steven F. Moss, Gerald Fraser, Eli Okon,Yaron Niv, Dept of Pathology, Beilinson Campus, Rabin Med Ctr,. Tel­Aviv Univ, Petach-Tikva, Israel; Dept of Gastroenterology, BeilinsonCampus, Rabin Med Ctr, Tel-Aviv Univ, Petach-Tikva, Israel; Gastroen­terology Div, St-Luke's-Roosevelt Hospital, Columbia University, NewYork, NY.

Introduction: Nine different genes for mucin have been described. MUC 5and MUC 6 encode the secreted apomucins of the stomach. A gradientfrom the surface epithelium (foveola) to the glands is typical for MUC 5synthesis, while a gradient in the opposite direction was found for MUC 6.Aim: To determine the distribution of MUC 5 and MUC 6 in the postoperative stomach, with relation to the H. pylori status. Metho.ds: Gastriccorpus biopsy specimens, from patients who underwent partial gastrec­tomy, were examined by immunohistochemistry for mucm gene (MUC 5and MUC 6) apoproteins. We used polyclonal antibodies for amino-acidtandem repeats of both proteins. A scoring system, 0-3, was used to assessstaining intensity at 4 sites: lumen, foveola, mucous neck cells and glands.

GASTROENTEROLOGY Vol. 118, No.4

H. pylori status was determined by histology and rapid urease test, andconsidered positive or negative when both tests were positive or negative,respectively. 19 H. pylori positive and 32 H. pylori negative patients werestudied. Results: No significant change in MUC 5 or MUC 6 synthesis andsecretion was demonstrated between H. pylori positive or negative patients.A gradient similar to that shown for the intact stomach (from the surfaceepithelium to the glands) for MUC 5 protein, and increase of MUC 6protein presentation from the mucous neck cell to the glands were dem­onstrated. Conclusion: The pattern of MUC 5 protein synthesis was notdifferent in H. pylori positive and negative patients in the post-operativestomach. MUC 6 expression was higher in the foveola in H. pylori positivepatients, whereas there was no difference in the other cell layers.

5841

HELICOBACTER PYLORI ERADICATION AND REFLUX OE·SOPHAGITIS IN PEPTIC ULCER AND DYSPEPTIC PATIENTSWITH OR WITHOUT HIATAL HERNIA.Sergio Morini, Vittorio Rinaldi, Angelo Zullo, Cesare Hassan, SalvatoreCampo, GI UNIT N REGINA MARGHERITA Hosp, Rome, Italy; DeptClin Med - Gastroenterol - La Sapienza Univ, Rome, Italy.

Background: It is still debated whether curing Helicobacterpylori infectionin patients with duodenal ulcer (DU) may provoke reflux oesophagitis.Moreover, few data exist on non-ulcer dyspepsia (NUD) or gastric ulcer(GU) patients. Aims: a) To confirm the previous observation of erosiveoesophagitis appearance after H. pylori eradication in DU patients, and toevaluate whether this event also happens in NUD and GU patients. b) Toevaluate whether hiatal hernia (HH) may playa role in the development ofreflux oesophagitis after H. pylori eradication Methods: This study enrolled122 patients (58 NUD, 44 DU, 20 GU) successfully cured for H. pyloriinfection. H. pylori eradication was assessed by a rapid urease test andhistology (Giemsa staining). Reflux oesophagitis rate was evaluated by afurther endoscopy at least 6 months later. Results: Before H. pylori erad­ication, 7 patients (4 NUD, 2 DU, 1 GU) presented erosive oesophagitisthat disappeared in 4 (57%) cases after eradication at the last conrol, On theother hand, erosive oesophagitis appeared in 7/115 (6.1%) of the remainingpatients during follow-up. In detail, 5/54 (9.2%) cases were observed inNUD patients, 2/42 (4.8%) cases in DU patients (p= NS), whilst no casewas observed amongst the 19 GU patients. Once excluded the 4 patientspreenting with erosive oesophagitis and HH at entry, erosive oesophagitisappeared in 5 out of 27 patients with HH (18%) and in 3 out of 9l (3%)without HH (p<0.002). Conclusions: This study found that H. pylorieradication is associated with a) disappearance of erosive oesophagitis inmore than half of the successfully cured patients, and b) appearance oferosive oesophagitis in both NUD and DU patients, without a statisticallysignificant difference between the two groups. HH plays a major role inreflux oesophagitis development after H. pylori eradication. Therefore, therole of H. pylori eradication in reflux oesophagitis must be further inves­tigated.

5842

HIGH NITRIC OXIDE LEVELS AT GASTRO·OESOPHAGEAL(GO) JUNCTION INDUCED BY DIETARY NITRATE. ?CAUSE OFMUTAGENESIS AT GO JUNCTION.Akihiko Moriya, Elaine B. Henry, Jeanette Grant, Jonathan Fletcher, CraigMowat, Craig Williams, Kenneth E. McColl, Univ of Glasgow, Glasgow,United Kingdom.

20% of absorbed nitrate is resecreted into saliva and 25% of this convertedto nitrite by buccal bacteria. On swallowing the nitrite is converted byacidic gastric juice containing ascorbic acid to nitric oxide (NO). AIM: Toinvestigate luminal concentrations of NO in different anatomical regions ofthe stomach following ingestion of 2mmol nitrate (equivalent to saladportion). METHODS: 9 healthy H. pylori negative volunteers were studiedfasted and following ingestion of 2mmol nitrate. A specially designedprobe incorporating two miniature NO sensors !Ocm apart and 4 pHsensors was passed perorally into the distal stomach. Following fluroscopicconfirmation of its position, the apparatus was slowly withdrawn over 90min with constant monitoring of NO concentration and pH, until it lay inthe oesophagus. RESULTS: Mean fasting salivary nitrite concentrationwas 40p,mol/l. During fasting NO concentrations in the upper GI tract weremaximal at the GO junction (median = 5p,mol/l, range 2-10) whereintraluminal pH first fell from neutral to <4. Following the nitrate meal,mean salivary nitrite concentration rose to 400p,mol/l and this was asso­ciated with a marked increase in intragastric NO levels. Maximal NO levelswere again observed at the GO junction. In 50% of the subjects steady stateNO levels greater than 30p,mol/l were recorded at the GO junction withlittle evidence of any NO production in the more distal stomach. CON­CLUSION: In a proportion of subjects the nitrite delivered in saliva is allconverted to NO as soon as it makes contact with acidic gastric juice. Thehigh levels of NO (known to be mutagenic) generated at the GO junctionmay explain the high incidence of mutagenesis at this anatomical region.