OMEPRAZOLE AMOXICILLIN - IMPAIRED ERADICA TION OF HELICOBACTER-PYLORIBY SMOKING BUT NOT BY OMEPRAZOLE PRETREATMENT/

Citation
G. Zala et al., OMEPRAZOLE AMOXICILLIN - IMPAIRED ERADICA TION OF HELICOBACTER-PYLORIBY SMOKING BUT NOT BY OMEPRAZOLE PRETREATMENT/, Schweizerische medizinische Wochenschrift, 124(31-32), 1994, pp. 1398-1404
Citations number
32
Categorie Soggetti
Medicine, General & Internal
ISSN journal
00367672
Volume
124
Issue
31-32
Year of publication
1994
Pages
1398 - 1404
Database
ISI
SICI code
0036-7672(1994)124:31-32<1398:OA-IET>2.0.ZU;2-T
Abstract
The efficacy of high dose omeprazole/amoxicillin (OME/AMOX) for eradic ation of Helicobacter pylori (HP) is controversial. Reported eradicati on rates range from 0% to 90%. Different therapy schedules and unknown factors may be crucial; in particular, pretreatment with OME has been thought to endanger HP eradication by subsequent OME/AMOX. Preliminar y findings suggested that smoking may impair eradication with OME/AMOX . The aims of this study were (1) to establish whether HP eradication rates differ depending on whether eradication with OME/AMOX was perfor med before or after ulcer therapy with OME, (2) to determine whether s moking impairs HP eradication by OME/AMOX and (3) to evaluate the effi cacy of OME/AMOX in our population. 52 HP positive outpatients with en doscopically documented recurrent duodenal ulcer were included. Exclus ion criteria were: alcoholism, previous gastric surgery, or intake of antibiotics, OME, bismuth salts, corticosteroids and NSAIDs within fou r weeks before study entry. Patients currently smoking >10 cigarettes/ day were classified as smokers. HP infection was confirmed by histolog y (3) biopsy specimens from the gastric antrum and 2 from the gastric body; H&E, Giemsa and at least positive rapid urease test (CLO) or cul ture. Eradication therapy consisted of oral OME (40 mg bid) and AMOX s olute (750 mg tid) for 10 days (OME/AMOX). This therapy preceded (grou p A) or followed (group B) ulcer therapy with OME (20 mg per day far 2 0 days). In group A 17 patients (2 females, 15 males, mean age 39 [19- 70]; 11 smelters, 6 nonsmokers) underwent ulcer therapy with OME (d 1- 20) before OME/AMOX d 21-30. In group B 35 patients (7 females, 28 mal es, mean age 42 [21-68]; 25 smokers, 10 nonsmokers) took ulcer therapy with OME (d 11-30) after OME/AMOX (d 1-10). Control endoscopy was don e after a minimal interval of 30 days from the end of treatment. Crite ria for eradication were negative CLO, failure to culture HP and failu re to visualize HP in histology of 3 antral and 2 gastric body biopsie s. Except for 2 patients with persistent HP infection, ulcer healing w as observed in all patients at control endoscopy. No patient dropped o ut because of side effects. Overall eradication rate was 35% (18/52). Eradication rates were, in group A, with OME pretreatment, 41% (7/17, in smokers 3/11 and in nonsmokers 4/6) and in group B, without OME pre treatment, 31% (11/35, in smokers 5/25 and in nonsmokers 6/10) respect ively (n.s.). In smokers the eradication rate of 22% (8/36) was signif icantly lower compared to 63% (10/16) in nonsmokers (p <0.02). (1) OME pretreatment did not impair HP eradication by subsequent OME/AMOX. (2 ) Cigarette smoking, however, significantly impaired eradication by OM E/AMOX. (3) In our population (with a proportion of 70% smokers) OME/A MOX eradicated HP in 35% of duodenal ulcer patients.