A140 AGA ABSTRACTS GASTROENTEROLOGY, Vol. 108, No, 4

DUODENAL ULCER HEALING: IS ONE-WEEK LOW-DOSE TRIPLE THERAPY SUFFICIENT? l.Labenz. R.J.Adamek, U.Peitz, B.Tillenburg, M.Wegener, J.P.Idstr~m, E.Rosen, G.Bi~rsch. Depts. of Medicine Elisabeth Hospital Essen and St.Josef-Hospital Bochum, Germany

Helicobacter pylori (H.pylori) is probably the most important factor in the pathogenesis of duodenal ulcer disease. The hypothesis was tested that one-week low-dose triple therapy is sufficient to heal duodenal ulcers. 1 Methods: Patients suffering from H.pylori-positive ( 3C-urea breath test) duodenal ulcers were treated wi th omeprazole 20 mg bid, Clarithromycin 250 mg bid and metronidazole 400 m g bid over one week. Patients were than randomized in a double-bl ind fashion to omeprazole 20 mg od or placebo for another three weeks. Ulcer heal ing was endoscojpicaUy checked after 2 and 4 weeks, the H.pylori-status a ~ n 8-10 weeks after enrollment to the s tudy by means of a ~ C-urea breath test. Patients: 59 pat ients were inc luded , One female patient ~ u e d eradication therapy prematurely because of mou th burning. The remaining patients were symptomfree after one week of eradication therapy. Up to now, ulcer heal ing was endoscopically observed after two weeks in 43 out of 50 patients (86%; 95%-CI: 73%-94%) and in all patients at tendin~ the 4-week visit (n=39). Side effects were rare and easily tolerated in all bu t onepat ient . Conclusion: Although the s tudy code was not broken by now, we conclude from our prel iminary data that one-week low dose triple therapy will be sufficient to heal the vast majority of duodenal Ulcers wi thin two weeks and almost all ulcers wi th in four weeks.

The s tudy was supported by a grant from AB Astra H~issle.

• EFFICACY AND SAFETY OF TWO SIMPLE ONE-WEEK TRIPLE THERAPY SCHEDULES FOR HELICOBACTER PYLORI. J.Labenz, R.J.Adamek, M.Stolte, W.Opferkueh, T.Becker, B.Tillenburg, G.B~rsch. Depts. of Medicine, Elisabeth Hospital Essen and St.Josef-Hospital Bochum, Germany.

Dual therapies containing omeprazole and amoxicillin cure Helicobacter pylori (H.pylori) infection, bu t the reported eradication rates varied rather widely. Therefore, we evaluated the eradication capability and safety of two novel triple therapies regimens for H.pylori. Methods: 120 consecutive patients suffer ing from histologically and/or culturally proven H.pylori infection and associated peptic ulcer disease (acute ulcer or disease in remission) (duodenal ulcer disease: n=69, gastric ulcer disease: n=21, gastroduodenal double ulcers: n=3) or functional dyspepsia (n=30) were treated over one week with either omeprazole 20 mg bid, amoxicillin 1 g bid and clarithromycin 250 mg b id (OAC; group I: patients 1-60) or with omeprazole 20 mg bid, amoxicillin 1 g bid and metronidazole 400 mg bid (OAM; group II: patients 61-120). H.pylori eradication was a s s e s s e d 4 weeks after discontinuation of the eradication therapy by means of urease test, culture and histology. Results: Three ~atients (OAC: n=l , OAM: n=2) were lost to ~ u p . On retention-to-treat analysis, H.pylori infection was cured in 53 out of 60 patients of group I (rate: 88% [95%- CI: 77%-95%]) and in 47 out of 60 patients of group II (rate: 78% ]95°/O-CI: 66%-88%]) without statistical significance between OAC and OAM (p=0.22). Nine patients of either group complained of side effects wi thout necessity of discontinuation of the s tudy medication (rates: 15% vs 15.5%; p=l.00). Conclusions: One-week simple triple therapy regimens consisting of omeprazole, amoxicillin and clarithromycin or metronidazole represent a sufficiently effective, well tolerated and simple approach to the cure of H.pylori infection. The eradication rates are somewhat lower than those obtained by omeprazole, clarithromycin and a nitroimidazole.

• INCIDENCE OF REFLUX ESOPHAGITIS AFTER CURE OF HELICOBACTER PYLORI INFECTION IN DUODENAL ULCER PATIENTS. J.Labenz, B.Tillenburg, U.Peitz, G.B~rsch. Dept. of Medicine, Elisabeth Hospital Essen, Germany.

Duodenal ulcer disease and reflux esophagit is are frequent ly associated disorders of the upper gastrointestinal tract. Up to now, only a few casuistic data are available on the incidence of reflux esophagitis after cure of duodenal ulcer disease by eradication of Helicobacter pylori (H.pylori). Mcthod~: 190 p a t i e n t s with formerly relapsing and/or complicated duodenal ulcer disease and without endoscopically visible signs of reflux esophagit is at the time of H.pylori eradication were prospectively followed for I to 4 years. Dur ing follow-up without any antiulcer drugs, patients were clinically and endoscopically reinvestigated in one-year intervals and when dyspeptic symptoms recurred. Dur ing each endoscopy, the H.pylori status was assessed by means of an urease test, culture and histology. Results: During follow-up of 316 patient years, 6 ulcer relapses occnred (rate: 1.9% per patient year), which were associated with either H.pylori recurrence (n=l), intake of ASS/NSAIDs (n=4), or cryptogenic liver cirrhosis (n=l). A total of 3 patients had H.pylorl recrudescence or reinfection, respectively, dur ing the first year after t reatment and none relapsed later (rate: 0.95% per patient year). Seventeen patients (rate: 8.9%) developped an endoscopicaUy proven reflux esophagitis, which was mild (grade I or II) in 16 patients and severe (ulcerative) in one female patient with stenosis of the duodenal bulb. Conclusions: H.pylori eradication cures duodenal ulcer disease in the long-term, but about 9% of patients will develop reflux esophagitis, which might be due to withdrawal of antisecretory drugs frequent ly used before eradication of H.pylori and/or a weight gain after cure of the infection and the associated ulcer disease.

ULCER HEALING BY ERADICATING HELICOBACTER PYLORI. J.Labenz, B.Tillenburg, M.Stolte, R.J.Adamek, T.Becker, G.Bi~rsch. Depts. of Medicine, Elisabeth Hospital Essen and St.Josef-Hospital Bochum, Germany.

There now exists convincing evidence that Helicobacter pylori (H.pylori) is a necessary, albeit by itself not sufficient factor in the pathogenesis of peptic ulcer disease (no H.pylori - no Ulcer). We tested the hypothesis that duodenal and gastric ulcers will heal spontaneously after an one-week eradication therapy. Methods: 112 patients with endoscopically proven duodenal ulcers (n=78), gastric ulcers (n=28), or gastroduodenal double ulcers (n=6) and associated H.pylori infection (histology/culture) were treated wi th one-week triple therapy regimens consisting of either omeprazole 20 m g od, clarithromycin 250 mg bid, and metronidzole 400 mg bid or tetracycline 500 mg b~d (OCM, OCT), or with omeprazole 20 mg bid, amoxicillin I g bid, and clarithromycin 250 m g bid or metronidazole 400 mg bid (OAC, OAM). Ulcer heal ing and H.pylori eradication (BUT, culture, histology) were assessed 4 weeks after cessation of the eradication therapy. Results: In all patients, symptoms referable to ulcer disease resolved within one week of treatment. The overall 5-week ulcer heal ing rate was 94.6% (106/112 patients; 95°/O-CI: 893o- 98%). Out o f these 106 patients, 96 have cured their infection and 10 demonstrated persist ing H.pylori infection. Ulcer heal ing was more frequently observed in patients wi th cure of H.pylori infection as opposed to the group of patients with persist ing bacterial colonization (97% vs 77%; p=0.02). Incomplete ulcer healing after 5 weeks was associated with either persistant H.pylori infection (n=2), intake of ASS/NSAIDs (n=5), or treatment with ASS 100 m g and H.pylori persistance (n=l): Conclusions: One-week, h ighly effective anti-H.pylori- treatment will in all l ikelihood be sufficient to heal duodenal and gastric ulcers, Treatment with antisecretory drugs after completion of eradication therapy should be reserved for patients with persistant symptoms and/or concomitant intake of uleerogenic drugs.