Helicobacter pylori eradication and reflux oesophagitis in peptic ulcer and dyspeptic patients with...
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A1278 AGA ABSTRACTS 5838 PHARMACOLOGIC CONCENTRATIONS OF VITAMIN C IN- HIBIT THE GROWTH OF HEUCOBACTER PYLORI IN VITRO. Anna U. Morgan, Mathew J. Domek, Univ High Sch, Irvine, CA; CA State Univ, Long Beach, CA. Research studies have demonstrated decreased concentrations of ascorbic acid in gastric juice of patients infected with Helicobacterpylori. In initial studies of physiologic concentrations of ascorbic acid, we found that vitamin C modestly decreased growth of H. pylori in vitro. The purpose of this study was to determine the effect of pharmacologic concentrations of vitamin C on growth of H. pylori in vitro. Pharmacologic concentrations of vitamin C are readily available from fresh fruits and from various vitamin preparations. METHODS: H. pylori were grown on 1.5% (w/v) plates prepared with 2.5% Brucella broth (w/v) and 10% fetal bovine serum (v/v) in the absence (control) and presence of varying concentrations from 50 p,g/mL to 5000 p,g/mL of vitamin C. types of vitamin C were I) vitamin C crystals, 2) Ester-C (calcium ascorbate) and 3) orange JUIce concentrate. The plates were inoculated with 100 p,L of a suspension of H. pylori in PBS containing approximately 100 cfu per plate. Plates were incubated at 37°C in 5% carbon dioxide. After four days the number of colonies of H. pylori on each plate was counted. RESULTS: At a concen- tration of 5000 p,g/mL, all three forms of vitamin C inhibited the growth of 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. pylori while 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. in vitro by I?ore than 99%. However, at lower, but equivalent, concentrations of vitamm C. orange juice is approximately 100-fold more potent than the other forms of vitamin C in inhibiting growth of H. pylori in vitro. studies need to be 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. 5839 DOES HELICOBACTER PYLORI EFFECT GASTRIC MUCIN EX- PRESSION? RELATIONSHIP BETWEEN GASTRIC MUCIN EX- PRESSION 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:,. Tel- Aviv Univ, Petach-Tikva, Israel; Dept of Gastroenterology, Beilinson Campus, Rabin Med Ctr, Tel-Aviv Univ, Petach-Tikva, Israel; Gastroen- terology 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. pylori infection causes aberrant expression of gastric mucins, MUC 5 and MUC 6. Aim: To determine the normal distribution of MUC 5 and MUC 6 in the stomach and to investigate changes in this pattern in the presence of H. pylori and after successful Methods: S'astric antrum. biopsy specimens were examined by immunohistochemistry for mucm gene (MUC 5 and MUC 6) expression. Polyclonal antibodies were used to detect amino-acid tandem repeats of each protein. A scoring system (0-3), was used to assess staining intensity at 4 sites: lumen, foveola, mucous neck cells and glands. H. pylori status was determined by histology and rapid urease test, and considered positive or negative when both tests were positive or negative, respectively. 49 patients positive for H. pylori, in .36 of whom successful eradication was performed, and 11 H. pylon negative patients were studied. Results: There was a gradient of MUC 5 expression, higher to lower. from the surface to the glands, which more pro- nounced before eradication. Increased MUC 5 synthesis m the mucous neck 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 mucous neck cells or foveola. MUC 6 was also secreted into the lumen and probably comprised the superficial part of the mucous layer. Conclusion: H. pylori may change mucous synthesis and secretion m the stomach. This phenomenon may facilitate H. pylori colonization. 5840 GASTRIC CORPUS MUCIN EXPRESSION AFTER PARTIAL GASTRECTOMY, IN RELATION TO COLONIZATION WITH HELICOBACTER PYLORI. Sara Morgenstern, Rivka Koren, Steven F. Moss, Gerald Fraser, Eli Okon, Yaron Niv, Dept of Pathology, Beilinson Campus, Rabin Med Ctr,. Tel- Aviv Univ, Petach-Tikva, Israel; Dept of Gastroenterology, Beilinson Campus, Rabin Med Ctr, Tel-Aviv Univ, Petach-Tikva, Israel; Gastroen- terology Div, St-Luke's-Roosevelt Hospital, Columbia University, New York, NY. Introduction: Nine different genes for mucin have been described. MUC 5 and MUC 6 encode the secreted apomucins of the stomach. A gradient from the surface epithelium (foveola) to the glands is typical for MUC 5 synthesis, 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 post operative stomach, with relation to the H. pylori status. Metho.ds: Gastric corpus biopsy specimens, from patients who underwent partial gastrec- tomy, were examined by immunohistochemistry for mucm gene (MUC 5 and MUC 6) apoproteins. We used polyclonal antibodies for amino-acid tandem repeats of both proteins. A scoring system, 0-3, was used to assess staining 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, and considered positive or negative when both tests were positive or negative, respectively. 19 H. pylori positive and 32 H. pylori negative patients were studied. Results: No significant change in MUC 5 or MUC 6 synthesis and secretion was demonstrated between H. pylori positive or negative patients. A gradient similar to that shown for the intact stomach (from the surface epithelium to the glands) for MUC 5 protein, and increase of MUC 6 protein presentation from the mucous neck cell to the glands were dem- onstrated. Conclusion: The pattern of MUC 5 protein synthesis was not different in H. pylori positive and negative patients in the post-operative stomach. MUC 6 expression was higher in the foveola in H. pylori positive patients, whereas there was no difference in the other cell layers. 5841 HELICOBACTER PYLORI ERADICATION AND REFLUX OE· SOPHAGITIS IN PEPTIC ULCER AND DYSPEPTIC PATIENTS WITH OR WITHOUT HIATAL HERNIA. Sergio Morini, Vittorio Rinaldi, Angelo Zullo, Cesare Hassan, Salvatore Campo, GI UNIT N REGINA MARGHERIT A Hosp, Rome, Italy; Dept Clin Med - Gastroenterol - La Sapienza Univ, Rome, Italy. Background: It is still debated whether curing Helicobacterpylori infection in 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 erosive oesophagitis appearance after H. pylori eradication in DU patients, and to evaluate whether this event also happens in NUD and GU patients. b) To evaluate whether hiatal hernia (HH) may playa role in the development of reflux oesophagitis after H. pylori eradication Methods: This study enrolled 122 patients (58 NUD, 44 DU, 20 GU) successfully cured for H. pylori infection. H. pylori eradication was assessed by a rapid urease test and histology (Giemsa staining). Reflux oesophagitis rate was evaluated by a further endoscopy at least 6 months later. Results: Before H. pylori erad- ication, 7 patients (4 NUD, 2 DU, 1 GU) presented erosive oesophagitis that disappeared in 4 (57%) cases after eradication at the last conrol, On the other hand, erosive oesophagitis appeared in 7/115 (6.1%) of the remaining patients during follow-up. In detail, 5/54 (9.2%) cases were observed in NUD patients, 2/42 (4.8%) cases in DU patients (p= NS), whilst no case was observed amongst the 19 GU patients. Once excluded the 4 patients preenting with erosive oesophagitis and HH at entry, erosive oesophagitis appeared 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. pylori eradication is associated with a) disappearance of erosive oesophagitis in more than half of the successfully cured patients, and b) appearance of erosive oesophagitis in both NUD and DU patients, without a statistically significant difference between the two groups. HH plays a major role in reflux oesophagitis development after H. pylori eradication. Therefore, the role of H. pylori eradication in reflux oesophagitis must be further inves- tigated. 5842 HIGH NITRIC OXIDE LEVELS AT GASTRO·OESOPHAGEAL (GO) JUNCTION INDUCED BY DIETARY NITRATE. ?CAUSE OF MUTAGENESIS AT GO JUNCTION. Akihiko Moriya, Elaine B. Henry, Jeanette Grant, Jonathan Fletcher, Craig Mowat, Craig Williams, Kenneth E. McColl, Univ of Glasgow, Glasgow, United Kingdom. 20% of absorbed nitrate is resecreted into saliva and 25% of this converted to nitrite by buccal bacteria. On swallowing the nitrite is converted by acidic gastric juice containing ascorbic acid to nitric oxide (NO). AIM: To investigate luminal concentrations of NO in different anatomical regions of the stomach following ingestion of 2mmol nitrate (equivalent to salad portion). METHODS: 9 healthy H. pylori negative volunteers were studied fasted and following ingestion of 2mmol nitrate. A specially designed probe incorporating two miniature NO sensors !Ocm apart and 4 pH sensors was passed perorally into the distal stomach. Following fluroscopic confirmation of its position, the apparatus was slowly withdrawn over 90 min with constant monitoring of NO concentration and pH, until it lay in the oesophagus. RESULTS: Mean fasting salivary nitrite concentration was 40p,mol/l. During fasting NO concentrations in the upper GI tract were maximal at the GO junction (median = 5p,mol/l, range 2-10) where intraluminal pH first fell from neutral to <4. Following the nitrate meal, mean salivary nitrite concentration rose to 400p,mol/l and this was asso- ciated with a marked increase in intragastric NO levels. Maximal NO levels were again observed at the GO junction. In 50% of the subjects steady state NO levels greater than 30p,mol/l were recorded at the GO junction with little evidence of any NO production in the more distal stomach. CON- CLUSION: In a proportion of subjects the nitrite delivered in saliva is all converted to NO as soon as it makes contact with acidic gastric juice. The high levels of NO (known to be mutagenic) generated at the GO junction may explain the high incidence of mutagenesis at this anatomical region.
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Transcript of Helicobacter pylori eradication and reflux oesophagitis in peptic ulcer and dyspeptic patients with...
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.
