CLINICAL COURSE OF DUODENAL-ULCER DISEASE ONE-YEAR AFTER OMEPRAZOLE PLUS AMOXICILLIN OR TRIPLE THERAPY PLUS RANITIDINE FOR CURE OF HELICOBACTER-PYLORI INFECTION
J. Labenz et al., CLINICAL COURSE OF DUODENAL-ULCER DISEASE ONE-YEAR AFTER OMEPRAZOLE PLUS AMOXICILLIN OR TRIPLE THERAPY PLUS RANITIDINE FOR CURE OF HELICOBACTER-PYLORI INFECTION, European journal of gastroenterology & hepatology, 6(4), 1994, pp. 293-297
Objective: To compare the medium-term clinical course of duodenal ulce
r disease after attempting to cure Helicobacter pylori infection with
either omeprazole (OME) plus amoxycillin (AMOX) or triple therapy plus
ranitidine. Design: Patients treated with OME/AMOX or triple therapy
plus ranitidine in a prospective, randomized and controlled study were
followed for 1 year. Patients and methods: A total of 40 patients wit
h active duodenal ulcer disease and H. pylori infection of the gastric
mucosa were randomly treated with either OME 26 mg twice daily plus A
MOX 500 mg four times daily for 2 weeks (group 1) or with bismuth subs
alicylate 600 mg, metronidazole 400 mg, tetracycline 500 mg, all three
times daily, and ranitidine 300 mg for 2 weeks (group 2). Study medic
ation was followed in both groups by a 4-week treatment course of rani
tidine 300 mg. After complete ulcer healing, patients were re-investig
ated clinically and with a C-13-urea breath test after 6 months. A cli
nical and endoscopic follow-up, including assessment of H. pylori infe
ction by urease test, culture and histology, and a C-13-urea breath te
st, was carried out after 1 year, or earlier, if symptoms recurred dur
ing the follow-up period. Results: One patient from each group was los
t to follow-up. H. pylori infection was cured in 15 out of 19 patients
in group 1 (78.9%) and in 16 out of 19 patients in group 2 (84.2%). H
. pylori reinfection was detected in one asymptomatic patient in group
2 after 1 year; 30 patients remained free of infection. Ulcer relapse
s were observed on endoscopy in three out of four patients with ongoin
g H. pylori infection following OME/AMOX treatment and in all three pa
tients in whom triple therapy failed to cure the bacterial infection (
P>0.1). Duodenal ulcer disease remained in remission in all patients w
ith successful H. pylori eradication compared with a 1-year ulcer rela
pse rate of 85.7% (six out of seven) in H. pylori-positive patients (P
<0.01). All patients with ulcer relapse were re-treated following cros
sover. H. pylori was eradicated in one out of three patients by triple
therapy and by OME/AMOX in a further three patients. Conclusions: OME
/AMOX seems to be equally as effective as triple therapy plus ranitidi
ne in eradicating H. pylori and healing duodenal ulcer disease. The me
dium-term natural course of ulcer disease is strongly dependent on the
presence or absence of H. pylori and is independent of the type of th
erapy used to eradicate the bacterial infection.