Volume 8 • Number 3 • 2003
H E L I C O B AC T E R
Helicobacter pylori Infection and Perforated Peptic Ulcer
Blackwell Publishing Ltd.
Prevalence of the Infection and Role of Antimicrobial
Treatment
Javier P. Gisbert and José María Pajares
Department of Gastroenterology. University Hospital of ‘La Princesa’, Madrid, Spain
ABSTRACT
Although the role of Helicobacter pylori infection
on noncomplicated peptic ulcer disease has been
definitively established, the precise relationship bet-
ween the organism and complicated ulcer has hardly
been studied. The mean prevalence of H. pylori infec-
tion in patients with perforated peptic ulcer is of
only about 65–70%, which contrasts with the almost
90–100% figure reported in noncomplicated ulcer dis-
ease. However, H. pylori infection rates in various
studies range markedly from 0% to 100%, sug-
gesting that differences in variables as number and
type of diagnostic methods used to diagnose
H. pylori infection, or frequency of nonsteroidal
anti-inflammatory drug intake, may be responsible
for the low prevalence reported in some studies.
Recurrent ulcer disease after peptic ulcer perforation
mainly occurs in patients with H. pylori infection,
which suggests that the microorganism plays an
P erforation accounts for more than 70% of
deaths associated with peptic ulcer disease,
mortality rates for perforated duodenal and
gastric ulcers being 0–10% and 10–40%, res-
pectively [1]. Overall, the operative mortality
for perforated peptic ulcer is ∼5% [2]. Simple
closure of a perforated peptic ulcer has been
compared with definitive surgery in several
randomized trials [2–4]. Ulcer recurrence has
been reported to occur in 61% and 6% of cases
following simple closure and definitive surgical
treatment, respectively, indicating that simple
closure by no means is sufficient to prevent ulcer
recurrence [5]. This high recurrence rate after
simple closure of the ulcer has been the basis for
arguments in favour of the addition of some
Reprint requests to: Javier P. Gisbert, M.D., Playa de Mojácar
29. Urb. Bonanza. 28669 Boadilla del Monte, Madrid,
Spain.
© 2003 Blackwell Publishing Ltd, Helicobacter, 8, 159–167
important role in this complication. All patients with
perforated peptic ulcer should be treated by simple
closure of the perforation and with therapy aimed at
healing of the ulcer and eradicating the H. pylori
infection, as disappearance of the organism prevents,
or at least decreases, ulcer recurrence and ulcer
perforation in patients with H. pylori-associated
perforated ulcers after simple closure. Therefore,
H. pylori eradicating treatment should be started
during the immediate postoperative period. The
patients with intractable recurrent symptoms of
peptic ulcer despite adequate medical treatment,
but without H. pylori infection (e.g. a patient using
nonsteroidal anti-inflammatory drugs), is probably
the only remaining indication for elective definitive
surgical treatment of peptic ulcer disease.
Keywords. Helicobacter pylori, peptic ulcer, peptic
ulcer perforation, perforated peptic ulcer.
surgical procedures. The conventional surgical
approach includes acid-reducing procedures,
such as partial gastrectomy or truncal vagotomy
with gastric outflow drainage. On the other
hand, with the advent of potent acid-suppressing
agents like proton pump inhibitors (PPI), more
patients are treated with simple patch repair and
maintained on long-term acid suppressing drugs,
although the effectiveness of this strategy in the
long term has been insufficiently studied [6,7].
Although the role of Helicobacter pylori
infection on noncomplicated peptic ulcer disease
has been definitively established, the precise
relationship between the organism and com-
plicated ulcer has hardly been studied [8].
H. pylori has been identified in noncomplicated
duodenal ulcer in a high proportion of the cases,
the figures being almost 100% in many studies,
with a mean prevalence value of ∼90%, especially
if previous NSAID intake or antibiotic use is
159
160 Gisbert and Pajares

excluded [9,10] (although, more recently, some
studies mainly performed in the USA have found
lower infection rates). However, the frequency
of H. pylori infection in perforated peptic ulcer
remains a matter of debate, as several authors
have reported lower prevalence of the infection
in patients with this complication. On the other
hand, the relationship between the presence of
H. pylori and the recurrence of the ulcer after
surgery and the possible advantage of eradica-
tion of the organism on this complication has not
been fully established. Our aim was therefore to
systematically review the studies assessing the
prevalence of H. pylori infection in patients with
perforated peptic ulcer, and to evaluate with
detail the role of the organism in the recurrence
of the ulcer or the ulcer perforation and, espe-
cially, the effect of eradication of the infection on
the recurrence of this important complication.
Bibliographical searches were performed in
the PubMed (Internet) database including stud-
ies available until March 2002, looking for the
following words (all fields): (Helicobacter pylori
OR H. pylori) and (‘perforated’ OR ‘perfor-
ation’). We also conducted a manual search of
abstracts from 1995 to 2001 from the Interna-
tional Workshop on Gastroduodenal Pathology
and Helicobacter pylori, and American Digestive
Disease Week. References of reviews on perfor-
ation in peptic ulcer disease, and from the articles
selected for the study, were also examined in
search of articles meeting inclusion criteria. Arti-
cles published in any language were included. The
prevalence of H. pylori infection in patients with
perforated peptic ulcer of each study was
recorded, as was the ulcer type (duodenal or
gastric) and the methods used to detect the
organism were also identified. Weighted mean
(taking into account the number of patients in
each study) of H. pylori prevalence and 95%
confidence interval was calculated. The effect of
eradication of the infection on the recurrence of
the ulcer or the ulcer perforation was assessed.
Prevalence of H. pylori infection in perforated
peptic ulcer
Only a few studies have evaluated the prevalence
of H. pylori infection in patients suffering from
perforated peptic ulcer. From the 19 studies
detailed in Table 1, including 1169 patients, a
mean prevalence (weighted mean) of only 68.1%
could be calculated (95% confidence interval,
65–71%) [11–28]. This figure is similar to that
reported in other ulcer complications, such as
gastric outlet obstruction [29]. Nevertheless,
more important is the information from
comparative studies, where the prevalence of

Patients Diagnosis of H. pylori

Table 1 Prevalence of H. pylori
Author (reference) (number) Ulcer type H. pylori prevalence (%) infection in studies of perforated
peptic ulcer
Reinbach et al. (11) 80 DU S 47
Sebastian et al. (12) 29 DU or GU 13UBT 83
Debongnie et al. (13) 36 DU or GU H, Cu, Ci 56
Ng et al. (14) 73 DU H 70
Lanas et al. (15) 29 DU S 76
Lanas et al. (15) 27 GU S 67
Matskura et al. (16) 21 DU S 95
Matskura et al. (16) 5 GU S 100
Chowdhary et al. (17) 15 DU RUT, Gram, Giemsa 0
Tokunaga et al. (18) 47 DU or GU I 92
Mihmanli et al. (19) 18 DU H 89
Chu et al. (20) 163 DU H 47
Sharma et al. (21) 44 DU or GU RUT, H 61
Omori et al. (22) 49 DU RUT, H, Cu 57
Metzger et al. (23) 47 DU or GU RUT 73
Oncel et al. (24) 52 DU 13UBT 75
Kate et al. (25) 202 DU S 73
Kate et al. (25) 60 DU RUT, H, S 53
Mendes et al. (26) 31 DU or GU RUT, Cu, Ca, 14UBT, S 100
Kumar et al. (27) 30 DU RUT, H 57
Tran et al. (28) 111 DU or GU RUT, H, S 96
DU: duodenal ulcer; GU: gastric ulcer; RUT: rapid urease test; H: histology; S: serology; UBT: urea breath
test; I: immunohistochemical stain; Cu: culture; Ci: citology; Ca: carbolfuchsin smear.
Overall H. pylori infection rate (weighted mean) including all studies (1169 patients) = 68.1% (95%
confidence interval = 65–71%).
Mean H. pylori infection rate in studies including only duodenal ulcers: 61.4%; and only gastric ulcers: 72.2%.

© 2003 Blackwell Publishing Ltd, Helicobacter, 8, 159 –167

H. pylori and Perforated Ulcer
H. pylori infection in cases with perforated
peptic ulcer is compared with that of the controls.
The first of these studies was performed by
Reinbach et al. [11], where the prevalence of
H. pylori in 80 patients presenting with acute
perforated duodenal ulcer was examined (by sero-
logy) and compared with age and sex matched
hospital control patients. Only 47% of the perfor-
ated duodenal ulcer patients were positive for
H. pylori and this was similar to the value
of 50% in the controls. Therefore, this was the
first study to conclude that the lack of associa-
tion of acute perforated duodenal ulcer and
H. pylori infection suggested that perforated
duodenal ulcer had a different pathogenesis
from chronic duodenal ulcer disease, and that
the first should not be regarded simply as a
complication of the second [11]. Consequently,
these findings suggested that other pathogenic
factors different from H. pylori should partici-
pate in perforated duodenal ulcer disease. Other
authors have reported that their prevalence of
56% in patients with perforated gastroduodenal
ulcers lay between that seen in age and sex
matched healthy blood donors (36%) and their
patients with uncomplicated peptic ulcers
matched for age, sex and ulcer location (86%)
[13]. Lanas et al. [15] studied 76 patients with
gastrointestinal perforation and 152 matched
controls. Independent risk factors for ulcer
perforation were smoking, alcohol, a history of
peptic ulcer and, especially, nonsteroidal anti-
inflammatory drug (NSAID) use; however, a
positive H. pylori serology was not demon-
strated to be a risk factor. Finally, some authors
have reported a higher density of H. pylori in
patients with perforated peptic ulcer than in
others with bleeding and stenotic ulcers [18].
However, other studies have not found signif-
icant differences between the perforated and
nonperforated peptic ulcer patients with respect
to H. pylori infection. Kate et al. [25] compared
the prevalence of H. pylori infection in patients
with perforated duodenal ulcer (after simple
closure) with that in controls, and could not
demonstrate statistically significant differences.
Matsukura et al. [16] conducted an age and
gender matched case-control study between
perforated and nonsurgical peptic ulcers in
H. pylori infection and examined differences
in the cytotoxin genes cagA and vacA. Serum
H. pylori IgG antibody was positive in 95% of
perforated vs. 93% of nonsurgical duodenal ulcers,
and in 100% of perforated vs. 86% of nonsurgical
© 2003 Blackwell Publishing Ltd, Helicobacter, 8, 159–167
161
gastric ulcer patients. There were no significant dif-
ferences between the perforated and nonsurgical
peptic ulcer groups for H. pylori cagA and vacA
markers, in agreement with a recent study [30].
Although the authors conclude from these
results that H. pylori infection is not etiologi-
cally related to perforation of peptic ulcer, this
study seems to demonstrate, in fact, that
H. pylori is probably the cause of almost all per-
forated and nonperforated ulcers, although the
organism is not responsible for the perforation
itself. In other words, uncomplicated and com-
plicated ulcers would be similar in terms of
H. pylori infection (both in prevalence and in
strain virulence), although the explanation for
the perforation of the ulcer only in some cases
remains unknown; these results suggest there-
fore that host factors are perhaps more relevant
pathogenic factors in perforation than H. pylori
infection itself.
Hypotheses to explain H. pylori-negative peptic
ulcer perforations
As previously shown, prevalence of H. pylori
infection in perforated peptic ulcer varies mark-
edly among studies, even when case-control
studies are considered. These controversial results
may be due, at least partly, to several factors,
as differences in frequency of NSAID use, the
type of the perforated ulcer considered (duo-
denal or gastric ulcer), the sensibility and specif-
icity of diagnostic methods of H. pylori, or the
possibility that the infection would have been
eradicated by procedures aimed to treat the ulcer
perforation.
NSAID Use
A possible explanation for the lower than
expected prevalence of H. pylori in some studies
of ulcer perforation may be the coexisting use of
NSAIDs, which constitutes a well-known inde-
pendent cause of ulcer complications. However,
most studies have not determined NSAID intake
prospectively using a structured questionnaire,
and have not reported prevalence of H. pylori
separately for patients with and without NSAID
intake. As an exception, in the study by Ng et al.
[14] the H. pylori infection rate demonstrated by
intraoperative and antral biopsies in patients
with perforated peptic ulcer was 70%, but this
figure rose to 80% if NSAID users were exclu-
ded (while in patients taking these drugs the
162
infection was detected in only 23% of the cases).
Other studies have reported a high proportion
of NSAID use in patients with peptic ulcer
perforation, especially in those uninfected [13],
suggesting that these drugs represent a relevant
factor associated with H. pylori-negative ulcer
perforations. Furthermore, some authors have
demonstrated that NSAID use is strongly
associated with an increased risk of upper gas-
trointestinal perforation, while H. pylori is not
different between patients with perforation and
controls [15]. Finally, it should be remembered
that even in patients refusing NSAID use we
cannot absolutely exclude the surreptitious use
of these drugs [15,31].
Ulcer Site (Duodenal or Gastric Ulcer)
H. pylori infection is the most important etio-
logic factor for noncomplicated duodenal ulcer,
where NSAIDs seem to play a less important role
[9,10,32]. However, the prevalence of H. pylori
infection in gastric ulcer disease is considerably
lower, suggesting that other factors different
from the organism – mainly NSAIDs – are res-
ponsible for a relatively high proportion of
ulcers located in the stomach [33]. As shown in
Table 1, most of the protocols have included
patients with duodenal or gastric ulcer disease in
the same study, and only a few studies have sepa-
rately studied the prevalence of the organism in
each peptic disease. Unexpectedly, mean H. pylori
infection rate in studies including only duodenal
ulcers was even lower (61%) than in those
including only gastric ulcers (72%), but in both
cases the prevalence was relatively low (Table 1).
Previous Use of Antibiotics
The course of intravenous antibiotics that are
routinely prescribed for patients with perforated
ulcer might eradicate H. pylori in some of these
patients. Thus, a single shot antibiotic treatment
with two antibiotics including metronidazole
in patients undergoing proximal gastric vago-
tomy was reported to be associated with eradic-
ation of H. pylori [34]. In this respect, some
studies that used serology – a method uninflu-
enced by the recent use of antibiotics – have
found prevalence rates of infection of almost
100% in perforated ulcers [16]. Nevertheless,
other studies could not confirm these results,
and reported relatively low infection rates even
with serology [11,25].
Gisbert and Pajares
Effect of Surgery on H. pylori Infection
Some authors have performed a systematic
review to answer the question whether surgery
for peptic ulceration eradicates H. pylori [35].
Among H. pylori-positive patients who had
undergone vagotomy alone the prevalence of
persistent H. pylori infection was of 83%, whereas
for partial gastrectomy it was only about 50%.
On one hand, these results indicate that, when
the true prevalence of H. pylori in ulcer perfora-
tion is to be assessed, infection status should be
evaluated before surgery, when the prevalence is
higher. On the other hand, the main clinical
implication of the persistently high prevalence
of H. pylori infection postoperatively is that
patients who have undergone surgery, parti-
cularly vagotomy, should be reviewed and
considered for antibiotic treatment that will cure
their chronic infection [35].
Diagnostic Methods
Finally, the number and type of diagnostic
methods to detect H. pylori may also be partly
responsible for the controversial results. Mendes
et al. [26] studied with detail a group of patients
with perforated peptic ulcer disease. After sur-
gery, the patients were submitted to endoscopy,
and H. pylori was searched by five different
methods including culture, rapid urease test,
carbolfuchsin smear, 14C-urea breath test, and
serology. The infection was demonstrated by at
least one test in 100% of the patients. Therefore,
the authors conclude that the use of several diag-
nostic methods allowed us to demonstrate that
H. pylori prevalence in perforated peptic ulcer
disease is similar to noncomplicated ulcer
disease. Similarly, Tran et al. [28] evaluated
H. pylori status in 111 patients by means of three
diagnostic methods (rapid urease test, histology
and serology), and reported an infection rate as
high as 96%.
In summary, the mean prevalence of H. pylori
infection in patients with perforated peptic
ulcer is only about 65–70%, which contrasts
with the almost 90–100% figure reported in
noncomplicated ulcer disease and also with the
higher frequency of the infection in other ulcer
complications, such as upper gastrointestinal
bleeding [36]. However, H. pylori infection rates
in various studies range markedly from 0% to
100%, suggesting that differences in variables as
number and type of diagnostic methods used to
© 2003 Blackwell Publishing Ltd, Helicobacter, 8, 159 –167
H. pylori and Perforated Ulcer
diagnose H. pylori infection, or frequency of
NSAID intake, may be responsible for the low
prevalence reported in some studies.
Based on the high prevalence of H. pylori
infection in patients not taking NSAIDs who
present with noncomplicated duodenal ulcer, it
could be argued that the probability of H. pylori
infection would be so high that, from a practical
point of view, it would not be necessary to
confirm the presence of the infection before
administering eradication therapy. In patients
with ulcer perforation, therapy could be started
intravenously immediately after the perforation is
diagnosed and the surgical procedure performed.
However, the multiple studies reporting low
prevalence of the infection in perforated ulcer
(Table 1) suggest, obviously, that ‘empirical’
antibiotic therapy without confirming H. pylori
infection cannot be generally recommended in
acute perforated ulcers [37]. We must not forget
the potential disadvantages of the ‘empirical’
strategy: cost and adverse effects of antibiotic
treatment in patients without the infection,
possible development of drug resistance also in
these patients, complications as a consequence
of the delayed diagnosis of diseases not caused by
the organism, and the false sensation of safeness
against future episodes of perforation when only
eradication therapy – without antisecretory
maintenance therapy – is prescribed. In conclu-
sion, H. pylori status should be determined when
the patients recover from the acute episode, by
either endoscopic biopsy or, if this exploration
is thought to be unnecessary, by serology or
13C-urea breath test.
Role of H. pylori in the recurrence of the ulcer or
the ulcer perforation
Primary treatment of a perforated ulcer involves
either patch closure or definitive surgery for the
ulcer. As previously mentioned, simple closure is
associated with an unacceptably high recurrence
rate of the ulcer [38]. On the other hand, defini-
tive surgery may have long-term side-effects in
patients who may otherwise have been cured by
simple closure alone [25]. Prescription of H2
receptor antagonists or proton pump inhibitors
with the intention to reduce ulcer recurrence
after simple patch closure has produced conflict-
ing results [6,7]. Therefore, the best therapy for
peptic ulcer perforation is still a matter of debate.
Peptic ulcer, and the perforation itself, may recur
after operation for perforation. It is uncertain,
© 2003 Blackwell Publishing Ltd, Helicobacter, 8, 159–167
163
however, why in some patients ulcers recur, whereas
in others they do not. Gastric acid secretion
and serum gastrin levels do not predict ulcer
recurrence in patients after simple closure of
perforation [39].
The role of H. pylori infection in the recur-
rence of the ulcer or the ulcer perforation in
patients with a history of perforated peptic ulcer
has been evaluated in some studies. Sebastian
et al. [12] identified H. pylori in most of the
patients who underwent simple closure of per-
forated peptic ulcer; 6 weeks later some patients
had an endoscopy performed, and persistence of
duodenal ulceration was demonstrated in seven
out of the 12 infected patients; from another
point of view, all patients with unhealed duode-
nal ulcer had H. pylori infection. Debongnie
et al. [13] studied the prevalence of H. pylori in
36 patients with a perforated ulcer; seven out of
the nine infected patients with a follow-up of at
least 12 months and no preventive treatment had
a symptomatic relapse; one patient without
H. pylori had a second perforation, the only
relapse in this group. Pescatore et al. [40] studied
six patients with ulcer perforation treated with
closure of the orifice by an omental plug and
H. pylori eradication regimen; at endoscopy
performed 1 month after surgery, all ulcers except
one had disappeared; in this patient, persistent
H. pylori gastritis was diagnosed and success-
fully treated by a second regimen with sub-
sequent ulcer healing at endoscopic evaluation
performed 2 months later. In the study by Chu
et al. [20] 163 patients with history of perforated
duodenal ulcer unrelated to NSAIDs underwent
upper endoscopy a mean of 74 months after
operation; recurrent duodenal ulcer was found
in 18% of the patients and these recurrences
were significantly related to H. pylori status.
Koyama et al. [41] studied a group of patients
with acute duodenal perforation; among the 42
patients who received nonoperative treatment,
three developed reperforation; endoscopic biopsy
or serum anti-H. pylori IgG measurement
confirmed the infection in all three patients.
Kate et al. [25] reviewed a group of 60 patients
5 years or more after perforation closure,
and found that 90% of patients with a recur-
rent ulcer had H. pylori infection compared
with only 19% in those with no ulcer. Finally,
Kumar et al. [27] studied 30 patients presenting
with perforated duodenal ulcer and who under-
went emergency laparotomy and simple omental
patch repair; upper gastrointestinal endoscopy
164
was done 11 weeks after surgery, when active
duodenal ulcer was present in 13 out of 17
patients with evidence of H. pylori infection and
in none of the noninfected patients.
In summary, recurrent ulcer disease after
peptic ulcer perforation mainly occurs in patients
with H. pylori infection, which suggests that the
microorganism plays an important role in this
complication.
Role of H. pylori eradication treatment in
perforated peptic ulcer
In previous years a tendency existed to perform
definitive surgery on perforated peptic ulcer.
However, in recent years, the theory that eradi-
cation of H. pylori decreases the rate of ulcer
relapse has resulted in a return to primary repair
with an omental patch over the perforated ulcer
[19]. Thus, as H. pylori infection seems to cause
ulcer recurrence after this complication, eradi-
cation of the organism is imperative after patch
closure [25]. The effect of H. pylori eradication
on the natural history of perforated peptic ulcer
has been addressed in a few studies. Ng et al. [42]
randomized patients with perforated duodenal
ulcers to receive either omeprazole alone or a
quadruple anti-H. pylori therapy. At 1-year follow-
up ulcer relapse was 38% in the omeprazole
group compared with only 5% in the group
receiving anti-H. pylori regimen. This study is
the first study examining the effect of H. pylori
eradication in patients with perforated duodenal
ulcer, and noteworthily demonstrates that after
H. pylori eradication, and without maintenance
acid-suppression agents, 95% of patients remain
ulcer-free at 1-year follow-up. Thus, the remis-
sion rate seems to be similar to that previously
reported in uncomplicated ulcers after H. pylori
eradication [43]. In the study by Alamowitch
et al. [44], 35 patients with perforated duodenal
ulcer were treated by simple closure, peritoneal
lavage and omentoplasty; no recurrence was
found after eradication of H. pylori with a
follow-up of 38 months. Metzger et al. [23]
prospectively studied 47 patients suffering from
acute peptic ulcer perforation and treated them
with simple closure and H. pylori eradication;
follow-up (median 43.5 months) revealed no
need for reoperation for peptic ulcer disease
and no mortality. Kate et al. [25] prospectively
followed 202 patients for 2 years after simple
closure of a perforated duodenal ulcer; patients
were randomized to receive either ranitidine
Gisbert and Pajares
alone or quadruple therapy (ranitidine, colloidal
bismuth subcitrate, metronidazole and tetracy-
cline) after operation; the authors showed that
the H. pylori infection rate was significantly
higher at all intervals of follow-up to 2 years in
patients with recurrent or residual ulcer after
closure of a duodenal ulcer compared with that
in patients in whom ulcer remained healed
(although the precise data of recurrence in the
ranitidine and in the H. pylori eradication group
were not given). Finally, Tran et al. [28] pre-
scribed an eradication regimen with omeprazole,
clarithromycin and amoxicillin to a group of
patients with perforated gastro-duodenal ulcer
treated with surgical suture; follow-up endo-
scopy was performed 4–6 weeks after treatment
cessation, when ulcer healing was demonstrated
in 93% of the patients.
It has been suggested that patients with peptic
ulcer that perforate be divided into those with
prior evaluation for H. pylori and appropriate
therapy for the ulcer and those without adequate
prior evaluation or treatment for the ulcer [45].
In the first group, H. pylori-negative patients
(both because they were initially H. pylori-
negative or because the organism has been eradi-
cated), an ulcer-definitive surgery should be
performed, as the cause of the perforation cannot
be attributed to the infection. Due to the impor-
tant role that H. pylori plays in peptic ulcer dis-
ease, it has even been suggested that the presence
or the absence of the infection may be assessed
at the time of perforation with a rapid serological
test (office-based test) and, thus, H. pylori-
negative cases could then be treated, as previously
mentioned, with ulcer-definitive surgery [45].
However, whole blood tests have achieved dis-
couraging results in many studies and they are,
at present, of doubtful usefulness [46].
On the other hand, when inadequate prior
evaluation or treatment of H. pylori infection
has been undertaken, three premises have been
considered, as suggested by Donovan et al.
[45] [1]: Most duodenal ulcers will be associa-
ted with H. pylori [2]. Ulcer-definitive surgery
should not be employed until an ulcer associated
with H. pylori infection has had the benefit of
H. pylori eradication therapy. And [3] treatment
at the time of perforation should be an assured
closure of the perforation, pending determina-
tion of H. pylori status. When the patient has
recovered from the consequences of the perfor-
ation, the status of H. pylori should be investi-
gated. If positive, H. pylori eradication regimen
© 2003 Blackwell Publishing Ltd, Helicobacter, 8, 159 –167
H. pylori and Perforated Ulcer
will be prescribed. Ulcer-definitive surgery
should be considered in an infected patient only
if there is relapse after appropriate eradication
therapy.
Based on previous findings, that H. pylori
eradication prevents ulcer recurrence in patients
with H. pylori-associated perforated ulcers, it
could be argued that maintenance antisecretory
therapy may not be necessary after confirming
eradication success. In other ulcer complications,
as upper gastrointestinal bleeding, it has been
reported in a recent meta-analysis comparing
the effect of H. pylori eradication with long-
term maintenance antisecretory therapy that
recurrent bleeding occurred in only 1% of
patients with H. pylori eradication success [47].
Nevertheless, in perforated ulcers there is less
information, and the role of maintenance anti-
secretory needs to be assessed in prospectively
comparative studies.
In summary, all patients with perforated
peptic ulcer should be treated by simple closure
of the perforation and with therapy aimed at
healing of the ulcer and eradicating the H. pylori
infection [48,49], as disappearance of the organ-
ism prevents, or at least decreases, ulcer recur-
rence and ulcer perforation in patients with
H. pylori-associated perforated ulcers after
simple closure. Therefore, H. pylori eradicating
treatment should be started during the immedi-
ate postoperative period [50]. The patients with
intractable recurrent symptoms of peptic ulcer
despite adequate medical treatment, but with-
out H. pylori infection (e.g. a patient using
NSAIDs), is probably the only remaining
indication for elective definitive surgical treat-
ment of peptic ulcer disease [5]. Nevertheless,
as H. pylori infection or NSAIDs are not the
cause for all peptic ulcer perforations, other thera-
peutic strategies might also be of major impact.
We are indebted to Brenda Ashley for assistance with
the English. Supported in part by a grant from the
Instituto de Salud Carlos III (C03/02).
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