The Effect of the Eradication of Helicobacter pylori
Infection on Hemorrhage Because of Duodenal Ulcer
Rinaldo Pellicano, M.D., Sergio Peyre, M.D., Nicola Leone, M.D.,
Alessandro Repici, M.D., Claudio De Angelis, M.D., Roberto Rizzi, M.D.,
Mario Rizzetto, M.D., and Antonio Ponzetto, M.D.
Abstract
The cost of a recurrently bleeding duodenal ulcer (DU) is very
high, both from a human and an economic point-of-view. Helico-
bacter pylori infection plays an important role in the pathogenesis
of DU disease and its complications, such as bleeding. Cure of H.
pylori infection is recommended in patients with DU and its com-
plications, although in the latter case, the most efficient manage-
ment is not yet a defined issue. In particular, acid secretion
inhibitors may not contribute to long-term cure. Our aims were to
ascertain whether the recurrence of bleeding because of DU could
be prevented by H. pylori eradication and whether long-term in-
hibition of gastric acid output is needed to prevent recurrence.
Eighty-four patients (65 men; mean age, 55.1 years), who had bled
because of recurrent DU, were followed after the cure of H. pylori
infection. None of the patients were on therapy with nonsteroidal
antiinflammatory drugs. Successful cure of H. pylori was deter-
mined by gastroscopy, histology, and serology performed at 3, 6,
12, 24, and 48 months after the eradication treatment. A
13
C urea
breath test was performed when the results of serology were un-
clear and also at recurrence of DU or bleeding. After the antibiotic
treatment, 46 patients stopped all medications, whereas 38 contin-
ued long-term therapy with histamine type 2 receptor antagonists.
During a mean follow-up period of 47.2 months (range, 37–65
months), recurrence of DU at endoscopy was observed in three
patients in each group (p 0.56), but none bled again. We con-
clude that H. pylori eradication prevents DU recurrence and re-
bleeding, that reinfection rate by H. pylori after cure was nil at 4
years, and that long-term inhibition of acid secretion may not
improve outcome after cure of H. pylori, even in patients whose
DU was complicated by hemorrhage.
Key Words: Helicobacter pylori—Duodenal ulcer—Bleeding—
Eradication.
A
bleeding duodenal ulcer (DU) is a costly event, both
from a human and an economic point-of-view. The
need for emergency endoscopy and for intensive care man-
agement imposes a severe burden on the health care system.
Helicobacter pylori infection plays an important role in the
pathogenesis of DU, and cure of the infection is known to
modify the natural history of the disease.
1
However, the
recurrence of bleeding DU raises questions such as whether
the rate of recurrence falls after H. pylori eradication,
whether long-term antisecretory treatment is needed, and
what the possibility of recurrence is. Our aim in this study
was to establish whether the eradication of H. pylori infec-
tion can reduce recurrence of both DU and rebleeding and
whether there is the need for long-term treatment with an-
tisecretory drugs.
MATERIALS AND METHODS
In a prospective, randomized study we included 84 patients (65
men) with a mean age of 55.1 years (range, 37–65 years) who had
had recurrent DU, documented by endoscopy, and who had bled
from the DU (Table 1). Bleeding was associated with the use of
nonsteroidal antiinflammatory drugs in none of the patients, and
we carefully instructed the patients to avoid the use of such com-
pounds during follow-up.
Presence of DU, bleeding, and recurrences were diagnosed by
upper gastrointestinal endoscopy performed at first diagnosis and
at 3, 6, 12, 24, and 48 months after cure of H. pylori, and every 2
years thereafter. Presence of bleeding was defined by the clinical
evidence of hematemesis or melena and by Forrest’s endoscopic
criteria.
2
During upper gastrointestinal endoscopy multiple biopsies
were obtained for histology. A serum sample was obtained from
each patient. All patients were infected by H. pylori. The presence
of H. pylori infection was diagnosed by histology (Giemsa stain-
ing) on biopsies obtained from the antrum and the fundus during
endoscopy and by measuring specific immunoglobulin G (IgG)
antibodies against H. pylori, by a commercial enzyme-linked im-
munosorbent assay. The infection was considered eradicated when
histology did not demonstrate the bacterium, either in antrum or
fundus, and the titer of circulating anti-H. pylori antibodies had
decreased by at least 50% of the initial value within 6 months of
cure of H. pylori.
The patients in whom levels of specific antibodies were not
halved within 6 months were offered a
13
C urea breath test (UBT),
performed according to the European Standard Protocol.
3
The
13
C
UBT was administered in cases of ulcer recurrence. After the cure
of H. pylori, 46 patients stopped medication, whereas 38 continued
the therapy with histamine type 2 receptor antagonists (ranitidine
150 mg/nocte) for the entire follow-up. All patients received upper
gastrointestinal endoscopy, histology, and serology as described
above. The
2
test and the Fisher exact test, when required, were
used for statistical analysis, and a p value of less than 0.05 was
considered significant. Odds ratios and 95% CI, assessing the risk
Submitted February 3, 2000. Accepted May 30, 2000.
From the Department of Internal Medicine (R.P., M.R.), University of
Turin, Turin, Italy; the U.O.A. Gastroenterology (S.P., R.R.), Cuorgné
Hospital, Cuorgné, Italy; and the Department of Gastroenterology (N.L.,
A.R., C.D.A., M.R., A.P.), Molinette Hospital, Turin, Italy.
Address correspondence and reprint requests to Dr. Rinaldo Pellicano,
Ambulatorio di Gastroenterologia, via Chiabrera 34, III piano, 10126
Turin, Italy. E-mail: rinaldo_pellican@hotmail.com
J Clin Gastroenterol 2001;32(3):222–224. © 2001 Lippincott Williams & Wilkins, Inc.
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