A278 AGA ABSTRACTS
GASTROENTEROLOGYVol. 114, No. 4
Gl140 CHANGE OF INTESTINAL METAPLASIA AFTER HELICOBACTER PYLORI ERADICATION: ASSESSMENT ACCORDING TO THE UPDATED SYDNEY SYSTEM. K, Satoh, K. Kimura, K. Kihira, T. Takimoto, and K. Tokumaru. Department of Gastroenterology, Jichi Medical School, Tochigi, Japan The aim of this study is to investigate the change of the severity of intestinal metaplasia (IM) in the antral and body mucosa after Helicobacter pylori eradication. Methods: The subjects included 15 patients who achieved H. pylori eradication (8 with atrophic gastritis, 5 with duodenal ulcers, and 2 with gastric ulcers, 6 males, mean age 51 yr). All patients underwent endoscopy, and biopsies were taken from the lesser and greater curvatures of the midantrum and middle body, and the lesser curvature of the incisura angularis of the stomach. The state of 1-1.pylori infection was assessed histologically (Giemsa stain). Histological severity of IM was graded as "no," "mild," "moderate," and "marked," according to the Updated Sydney System, and scored on a 0-3 scale (using hematoxylin and eosin, Alcian blue/periodic acid Schiff, and high iron diamine/Alcian blue stains). The patients were followed for 12-33 (mean 18) months after anti-/-/, pylori therapy. The IM scores were compared between before and after eradication (at the end of follow-up), using one sample Wilcoxon test. Results: The IM scores before and after eradication were shown: Antrum Body score
efficacy of three short-term therapies in relation to the prevalence of metronidazole and clarithromycin reistance in a given area. Methods. So far, 119 consecutive H. pylori-positive dyspeptic patients have completed this randomized, two-center, open, parallel-group study. They were subdivided into three arms receiving the following 1-week regimen: 1) Ranitidine bismuth citrate 400 mg bd + clarithromycin 250 mg bd + metronidazole 500 mg bd (RBCCM), 2) Bismuth subcitrate 240 mg bd + amoxicillin 1000 mg bd + metronidazole 500 mg bd (BAM), 3) Omeprazole 20 mg od + clarithromycin 250 mg bd + metronidazole 500 mg bd (OCM). H. pylori was assessed by CLO-test and histology on both antral and corpus biopsies before and at least 4 weeks after the end of therapy. The bacterium was considered eradicated when both tests were negative. Biopsy specimens from antrum and corpus were taken for culture and primary resistance to metronidazole and clarithromycin were assessed by E test. Chi-square test and 95% CI were used for statistical analysis. Results. They are reported in the table: REGIMEN RBCCM BAM OCM
INTENTION-TO-TREAT (95% C1) PER-PROTOCOL(95%CI) 34/39 = 87% (73-96) 34/36 = 94% (81-99) 30/40 = 75% (59-87) 30/36 = 83% (67-94) 21140 = 52% (36-68) 21/33 = 63% (45-80)
The best eradication rates have been achieved with RBCCM, which is more effective than BAM (p=NS) and significantly better than OCM (p < 0.003), using both intention-to-treat and per protocol analysis. So far, we have analyzed by culture and E test 45 biopsy specimens from our patients. Culture was successful in 35 out of them and 17135 (48%) were resistant to rnetronidazole (MIC > 8 lag/mL) and 4•33 (12%) to clarithromycin (MIC > 2 lag/mL). No patient dropped out because of serious adverse events in any of the three groups. Side effects were registered in 17%, 20% and 15% of cases, respectively. Conclusions. Bismuth-based 7-day triple therapies seem to be more effective than the omeprazole-based triple regimen. In particular, RBCCM produces significantly better results than OCM. The high prevalence of antibiotic resistance in our geographical area seems to affect much more omeprazole-based than ranitidine bismuth citrate-based triple therapy.
Antral IM developed in four of 10 patients. Body IM developed in two and regressed in four patients, who had it at the lesser curvature only. Conclusions: During the follow-up of 1-3 years after H. pylori eradication, we found no marked improvement of antral IM. It developed in 40% of patients. As to body IM, development and regression were found.
Gl143 CLASSIC SYMPTOMS ARE HIGHLY PREDICTIVE OF GASTROESOPHAGEAL REFLUX DISEASE (GERD). V. Saxena. L. Fiennes, J.M. Bland, T.C. Northfield, P.J. Howard. St. George's Hospital Medical School, Tooting, London, England.
• Gl141 ?A-HOUR GASTRIC PH AND DUODENAL GASTRIC METAPLASIA ONE YEAR AFTER ERADICATION OF HELICOBACTER PYLORI INFECTION IN DUODENAL ULCER PATIENTS. V. Savarino, G.S. Mela, P. Zentilin, M.R. Mele, G. Bisso, M. Pivari, C. Mansi, G. Lapertosa, P. Ceppa, *S. Vigneri, G. Celle. Gastroenterology Unit, DI.M.I., University of Genoa and *Institute of Internal Medicine and Geriatrics, University of Palermo, Italy.
Background: Classic symptoms are regarded as too imprecise to identify patients with gastro-esophageal reflux disease (GERD) and invasive techniques such as endoscopy and pH monitoring are regarded as necessary to make an accurate diagnosis. Aim: To assess prospectively the value of classic symptoms in the diagnosis of GERD, and to identify which symptoms are the most predictive. Methods: 37 patients referred for open access endoscopy were recruited after informed consent. All subjects completed a detailed symptom questionnaire. Reflux symptoms were grouped into atypical (Group A-lower abdominal pain, abdominal rumbling, bloating, diarrhoea, constipation, pain eased by passing wind/opening bowels, pale stools), non-specific (Group B-nausea, upper abdominal pain, vomiting, fullness, belching) and classic (Group C-heartburn, acid in mouth, waterbrash, food regurgitation, odynophagia, dysphagia for solids, pain on swallowing hot liquid/alcohol, pain on stooping/bending, pain after food). All underwent endoscopy, esophageal manometry, 24 hour ambulatory pH monitoring and a Bemstein acid perfusion test. Symptomatic GERD was defined as a symptom reflux association of > =50% or a positive Bernstein test in those who were asymptomatic during the 24 hour pH study. Patients were divided into those with and without symptomatic GERD and odds ratios were calculated for each of the above symptoms. Results: 22 of the 37 patients fulfilled the criteria for symptomatic GERD. For Group C symptoms the odds ratios were: acid in mouth-84.3, heartburn64.8, pain worse on stooping/bending/lying-41.4, food regurgitation-29.0, waterbrash-23.0, pain on swallowing hot liquid/alcohol-23.0, odynophagia10.3, dysphagia for solids-6.27, pain after food-l.94. For group B symptoms only belching was significant (13.5). None of the Group A symptoms produced significant odds ratios except abdominal rumbling (5.80). There was no significant difference (p=0.76) in the total number (expressed as median, range) of group A symptoms between those with GERD (2.00, 0-4) and those without GERD (2.00, 0-5). However, the total number of Group B symptoms in the GERD patients (3.00, 2-5) was significantly greater than the non-GERD group (2.00, 1-4); p=0.007. This was also the case for Group C symptoms: GERD group (5.00, 0-6), non-GERD group (1.00, 0-1); p < 0.000!. 20/22 of the GERD group had 2 or more group C symptoms, whereas all 15 of the non GERD group had less than 2 group C symptoms. The presence of 2 or more Group C symptoms predicted symptomatic GERD with a 91% sensitivity, 97% specificity and 95% accuracy. Condusion: Classic symptoms are highly predictive of gastro-esophageal reflux disease, with the exception of pain after food. The presence of two or more classic symptoms is virtually diagnostic and the absence of any classic reflux symptoms virtually excludes the condition. An accurate diagnosis of symptomatic GERD can reliably be made on the history. This project was generously funded by Wyeth Laboratories, UK.
It is not clear whether duodenal gastric metaplasia (DGM) can be reversed by the eradication of Helicobacter pylori (Hp) infection and by the normalization of the germ-induced alterations in gastric physiology. For this reason, we evaluated the circadian pattern of gastric acidity and the extent of DGM before and one year after Hp eradication in a group of duodenal ulcer patients. Methods. 15 patients with endoscopically-proven Hp+ve duodenal ulcer (12 M and 3 F, median age 53, ranges 35-71 yrs) were recruited for this study. Hp infection was assessed by histology and DGM was diagnosed on four bulb biopsies taken before and one year after Hp eradication. At the same times gastric pH was measured by 24-hour continuous intraluminal recording. Hp eradication was confirmed by negative CLO-test and histology performed both 4 weeks after the end of a treatment combining omeprazole 20 mg bd plus amoxicillin 1 gr bd and metronidazole 500 mg bd for 1 week and at the 1-year endoscopic control. After successful cure, all patients discontinued any antiulcer medication. Mean gastric pH was calculated over 24 hours and compared by ANOVA and changes in DGM were analysed by the sign test. Correlation between gastric pH and DGM was assessed by non-parametric covariance analysis. DGM on biopsy specimens was assessed by two experienced pathologists, who showed excellent agreement before eradication (k=0.88) and after 1 year (k=0.91). Results. 24-hour gastric pH was 1.7 _+0.4 before and 1.6 -+ 0.4 after 1 year of Hp eradication (p=NS). DGM resulted improved in 3 cases, worsened in 4 cases and unchanged in 8 cases at the 1-year control (p=NS). No correlation was found between 24-hour gastric pH and DGM (p=NS) at baseline and after 1 year. Conclusions. Our results show that neither gastric acidity nor DGM change significantly 1 year after Hp eradication in duodenal ulcer patients. Thus, the disappearance of Hp infection does not determine any reversal of gastric-type epithelium in the duodenum. • Gl142 A COMPARISON OF THREE 7-DAY TRIPLE REGIMENS IN THE ERADICATION OF HELICOBACTER PYLORI INFECTION. PRELIMINARY RESULTS. V. Savarino, G. Bisso, M. Pivari, C. Bilardi, M.IL Mele, °A. Costa, G.S. Mela, P. Zentilin, C. Mansi, P. Borro, °°G. Borgonovo, °°L. De Salvo, • S. Vigneri, G. Celle. DI.M.I., °Inst. of Microbiology and °°SurgicalClinic, Univ. of Genoa and *Inst. of Int Medicine and Geriatrics, Univ. of Palermo, Italy. One-week triple regimens are currently the most recommended therapy for the eradication of Helicobacter pylori. No previous study has compared the