| Literaturrecherche Ätiologie
Ulkuskrankheit |
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"Stand
des Irrtums" ca Juli 2004 |
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| Ätiologie UlkusKH
allgemein |
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Helicobacter pylori, non-steroidal
anti-inflammatory drugs and smoking in risk
pattern of gastroduodenal ulcers. |
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Scand
J Gastroenterol. 2003 Sep;38(9):923-30. |
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PMID:
14531527 [PubMed - indexed for MEDLINE] |
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Konturek
SJ, Bielanski W, Plonka M, Pawlik T, Pepera J,
Konturek PC, Czarnecki J, Penar A, Jedrychowski W. |
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Dept.
of Physiology, University College of Medicine,
Cracow, Poland. mpkontur@cyf-kr.edu.pl |
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BACKGROUND: Helicobacter pylori,
NSAID and cigarette smoking are major risk
factors for gastroduodenal ulcers. However, the
results of studies on the interaction between
these factors on ulcerogenesis are controversial.
This study was designed to examine the
association between gastroduodenal ulcers and H.
pylori infection, NSAID use, smoking and age.
METHODS: 5967 dyspeptic patients underwent 13C-urea
breath test (UBT) and upper endoscopy, while age
and dyspeptic symptoms were reported.
RESULTS: Out of 5967 patients, 31.8% were
ulcerated; 9.2% had gastric, 17.2% duodenal and 5.4%
both gastric and duodenal ulcers. H. pylori was
found in 72.5% of gastric ulcer patients, in 83.6%
of duodenal ulcer patients, in 76.9% of
gastroduodenal ulcer patients and in 64.8% of
dyspeptic patients. The gastric, duodenal and
gastroduodenal ulcers were related to H. pylori
significantly and the respective ORs were: 1.44,
2.77 and 1.81. NSAID alone was
used by 6.2%-12.7% of ulcer patients, tending to raise
only the risk of gastric ulcer but
reducing that of duodenal and gastroduodenal
ulcers. The H. pylori prevalence was
significantly higher in smokers (76%) than in non-smokers
(67%) and the ulcer risk was also
significantly higher in smokers than in non-smokers.
About 20% of ulcers were 'idiopathic', i.e.
without NSAID and H. pylori and the ratio of
these ulcers to all ulcers significantly
increased during the 5 years of the study.
CONCLUSIONS: Based on multivariable logistic
regression analysis we conclude that: 1) H.
pylori infection, NSAID use, smoking and age play
major roles in the pathogenesis of peptic
ulcerations; 2) there is a negative
interaction between H. pylori and NSAID on
duodenal ulcers, suggesting that H. pylori
reduces the development of these ulcers in NSAID
users, and 3) about 20% of peptic ulcers
in the Polish population are unrelated to H.
pylori and NSAID use (idiopathic ulcers). |
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The prevalence of
peptic ulcer not related to Helicobacter pylori
or non-steroidal antiinflammatory drug use is
negligible in southern Europe |
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Helicobacter.
2004 Jun;9(3):249-54. |
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PMID:
15165261 [PubMed - indexed for MEDLINE] |
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Arroyo
MT, Forne M, de Argila CM, Feu F, Arenas J, de la
Vega J, Garrigues V, Mora F, Castro M, Bujanda L,
Cosme A, Castiella A, Gisbert JP, Hervas A, Lanas
A. |
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Service
of Gastroenterology, Hospital Clinico, Zaragoza,
Spain. |
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BACKGROUND AND AIM: Helicobacter
pylori is the major cause of peptic ulcer
disease, but the proportion of H. pylori-negative
peptic ulcers seems to be increasing in developed
countries. We investigated the frequency of H.
pylori-negative peptic ulcer without intake of
nonsteroidal anti-inflammatory drugs (NSAIDs) in
a Mediterranean European country.
MATERIALS AND METHODS: We prospectively collected
consecutive patients with an endoscopically
verified active peptic ulcer over 6 months from
different areas of Spain. Helicobacter pylori
infection was assessed by rapid urease test and
histologic examination (corpus and antral
biopsies). A (13)C-urea breath test was performed
if H. pylori was not detected with the invasive
test. Patients were considered H. pylori-negative
if all three tests were negative. NSAID use was
determined by structured data collection.
RESULTS: Of 754 consecutive peptic ulcer
patients, 16 (2.1%) were H. pylori-negative and
had not used NSAIDs before the diagnosis. Of the
472 patients who had duodenal ulcers, 95.7% (n =
452) were H. pylori-positive and only 1.69% (n =
8) were negative for both H. pylori infection and
NSAID use; 193 patients had benign gastric ulcers
and 87% (n = 168) of them were infected by H.
pylori (p <.001 vs. duodenal ulcers). NSAID
intake was more frequent in gastric ulcer
patients (52.8%) than in duodenal ulcer
patients (25.4%; p <.001). Consequently, the
frequency of H. pylori-negative gastric ulcer in
patients not using NSAID was 4.1% (n = 8).
CONCLUSION: Peptic ulcer disease is still
highly associated with H. pylori infection
in southern Europe, and only 1.6% of all duodenal
ulcers and 4.1% of all gastric ulcers were not
associated with either H. pylori infection or
NSAID use. |
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FullText als PDF |
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Multivariate analysis
of risk factors for development of duodenal ulcer
in Helicobacter pylori-infected patients. |
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Digestion
2003;67(1-2):25-31 (ISSN: 0012-2823) |
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Regula
J; Hennig E; Burzykowski T; Orlowska J;
Przytulski K; Polkowski M; Dziurkowska-Marek A;
Marek T; Nowak A; Butruk E; Ostrowski J |
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Department
of Gastroenterology, Medical Center for
Postgraduate Education, Warsaw, Poland. |
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BACKGROUND: Although Helicobacter
pylori is a significant etiologic factor of
peptic ulcer disease, it remains unknown why
ulcers develop only in the minority of infected
individuals. AIM: The aim of this cross-sectional
study was to evaluate the association between the
presence of duodenal ulcer in H. pylori-infected
patients and different risk factors.
METHODS: A total of 122 H. pylori-infected
patients were enrolled; 79 had duodenal ulcer and
43 gastritis. Univariate analysis was conducted
using either Fisher's exact test or exact
Cochrane-Armitage trend test. In multivariate
analysis the logistic model was used.
RESULTS: Univariate analysis indicated six
factors (male sex, smoking, antral H.
pylori density, CAGA presence in antrum,
and VACA s1a presence in antrum and corpus). Four
factors (sex, smoking-alcohol index, H. pylori
density index, and CAGA index) were found to be
significant in multivariate analysis. The best
model predicting duodenal ulcer included male
sex, smoking, presence of H. PYLORI on
histopathology in antrum and CAGA presence in
corpus.
CONCLUSION: Although several risk factors were
significantly associated with duodenal ulcer, we
failed in the identification of either a single
risk factor or a set of factors that can
unequivocally differentiate patients with ulcer
from those with gastritis. [Copyright 2003 S.
Karger AG, Basel]. |
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What role today for
Helicobacter pylori in peptic ulcer? |
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Gastroenterol
Clin Biol 2003 Mar;27(3 Pt 2):409-14
(ISSN: 0399-8320) |
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Cadiot
G |
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Service
d'Hepato-Gastroenterologie, Hopital Robert-Debre,
51092 Reims Cedex. gcadiot@chu-reims.fr |
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Helicobacter pylori (H. pylori)
and nonsteroidal anti-inflammatory drugs/aspirin
(NSAIDs) remain today the main etiologies of
duodenal (DU) and gastric (GU) ulcers. In some
countries or areas in which prevalence of H.
pylori infection has decreased, and probably also
in which the consumption of NSAIDs is high, the
proportion of ulcers not associated with H.
pylori is high. Nevertheless, the proportion of
Helicobacter pylori-negative, NSAID-negative
ulcers remains low, less than 6% in most studies.
Furthermore, this proportion is probably
overestimated because the search for the
infection and NSAIDs treatments was not always
performed properly. Data about characteristics of
idiopathic GU (after excluding cancer) are
missing. In two studies, Helicobacter pylori-negative,
NSAID-negative DU were
associated in two thirds to three quarters of the
cases with co-morbidities, often
severe (cirrhosis, respiratory, renal or cardiac
failure, malignancy). Numerous digestive diseases
can give a DU, Crohn's disease
being probably the most frequent one. Gastric
acid hypersecretion, as in H. pylori-positive
DU, seems to be the pathogenic factor of
idiopathic DU, with increased duodenal acid load.
The outcome of idiopathic ulcers has been little
studied. There are no reliable data concerning
the risk of complications. Therapy is based on
proton pump inhibitors at a dosage allowing
prolonged healing. |
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Present position in
the prevention and therapy of NSAID-induced
ulcers |
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Schweiz
Med Wochenschr 1999 Jul 27;129(29-30):1073-80
(ISSN: 0036-7672) |
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Lehmann
FS; Beglinger C |
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Abteilung
fur Gastroenterologie, Universitatsspital Basel. |
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The administration of nonsteroidal
anti-inflammatory drugs (NSAIDs)
is frequently associated with injury to the
gastroduodenal mucosa and leads in approximately 1.5%
of patients to severe complications such
as haemorrhage or perforation. The risk of
serious upper GI complications is increased in
patients > 65 years with a
previous history of peptic ulcer disease or
gastrointestinal haemorrhage, concomitant steroid
use and significant cardiovascular comorbidity.
Previous studies have shown that misoprostol is
effective in reducing the incidence of gastric
and duodenal ulcers as well as serious
gastrointestinal complications. Recently, four
large clinical trials have demonstrated that
omeprazole is effective in preventing and
treating NSAID-induced ulcers. Omeprazole
when compared to misoprostol was equally
effective in preventing gastric ulcers and more
effective in duodenal ulcers. For treatment of
gastric and duodenal ulcers, omeprazole was more
effective than misoprostol and ranitidin.
Prophylaxis of NSAID-induced ulcers should be
administered in all patients with several risk
factors for serious gastrointestinal
complications. |
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H. pylori-negative
duodenal ulcer prevalence and causes in 774
patients |
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Dig
Dis Sci 1999 Nov;44(11):2295-302
(ISSN: 0163-2116) |
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Gisbert
JP; Blanco M; Mateos JM; Fernandez-Salazar L;
Fernandez-Bermejo M; Cantero J; Pajares JM |
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Department
of Gastroenterology, University Hospital La
Princesa Madrid, Spain. |
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The prevalence of H. pylori
infection has been reported to be very high in
duodenal ulcer (DU) disease, but the precise
frequency and causes of H. pylori-negative DU are
not well known. In some geographical regions,
however, a relatively low prevalence of the
infection has been described. Our aim was to
study the frequency and causes of H. pylori-negative
DU and to evaluate whether empirical H. pylori
eradication therapy without confirmation of the
infection is justified. In all 774 consecutive
patients with an endoscopic diagnosis of DU were
studied prospectively. Exclusion criteria were
associated diseases and previous gastric surgery.
The use of NSAIDs, antibiotics (during the last
month), and proton pump inhibitors (during the
last month) was evaluated by means of a specific
questionnaire. At endoscopy, two biopsies from
both antrum and corpus were obtained in all 774
patients for histologic study (H&E stain).
One sample from the antrum for rapid urease test,
one sample each from the antrum and corpus for
culture, and two duodenal biopsies for histologic
study were also obtained in the first 307
patients. A [13C] urea breath test was carried
out in the remaining 467 patients. Patients were
considered infected if any of the diagnostic
tests were positive and noninfected when all
tests performed were negative. Age (mean +/- SD)
was 46+/-12 years, 70% were males. NSAID,
antibiotic, and proton pump inhibitor use was
described, respectively, in 8.9%,
5.8%, and 6.3% of the cases. H. pylori infection
was demonstrated, overall, in 95.3% (95% CI: 93.6-96.6%)
of the patients. H. pylori prevalence increased
up to 99.1% (98.1-99.6%) if patients taking
NSAIDs and/or antibiotics were excluded. Among
the 36 H. pylori-negative patients, 20 (55%) were
taking NSAIDs, 9 (25%) were taking antibiotics,
and 1 (3%) both of them. Therefore, in only 6/774
patients (0.8%) could DU disease be considered
truly "idiopathic." Differences were
demonstrated between H. pylori-positive and -negative
patients (univariate study; chi2) with regard to
NSAID intake (7% vs 58%; P < 0.0001) and
previous antibiotic use (5% vs 28%; P < 0.0001).
In the multivariate analysis (logistic regression),
NSAID use (OR: 0.06; CI: 0.03-0.13; P < 0.001)
and antibiotic use (OR: 0.23; CI: 0.09-0.59; P
< 0.01) were the only variables that
correlated with H. pylori infection. The most
important factors associated with H. pylori-negative
DU are NSAIDs and prior antibiotic use, and if
these agents are excluded, the prevalence of
infection in our area is as high as 99%.
Therefore, in DU patients not taking NSAIDs and
living in areas where previous studies have shown
the prevalence of the infection in DU disease to
be very close to 100%, empirical H. pylori
eradication therapy without confirmation of the
infection may be justified. |
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| Ulkus sowie
Helicobacter bezw. NSAR |
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Impact of Helicobacter
pylori and nonsteroidal anti-inflammatory drugs
on gastric ulcerogenesis in experimental animals
and in humans. |
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Eur
J Pharmacol 2002 Aug 2;449(1-2):1-15
(ISSN: 0014-2999) |
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Pawlik T;
Konturek PC; Konturek JW; Konturek SJ; Brzozowski
T; Czesnikiewicz M; Plonka M; Bielanski W; Areny
H |
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Department of
Physiology, University Medical College, Ul.
Grzegorzecka St. 16, 31-531, Cracow, Poland. |
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Helicobacter
pylori (H. pylori) and nonsteroidal anti-inflammatory
drugs (NSAID) are the most common pathogens in
the gastroduodenal mucosa in animals and humans,
but their relationship in ulcerogenesis has been
little studied. According to some authors, H.
pylori infection in humans does not act
synergistically with NSAID on ulcer healing,
therefore, there is no need to eradicate the germ.
This notion is supported by the finding that the eradication
of H. pylori does not affect NSAID-induced
gastropathy treated with omeprazole and
that H. pylori infection induces a strong
cyclooxygenase-2 expression resulting in
excessive biosynthesis of gastroprotective
prostaglandins, which should in turn counteract
NSAID-induced gastropathy and heal the existing
ulcer. Other investigators claim that H. pylori
infection acts synergistically with NSAID on
ulcer development, therefore, H. pylori should be
eradicated, particularly at the start of long-term
NSAID therapy. Maastricht 2-2000 consensus also
recommends eradication prior to NSAID treatment,
but this eradication does not appear to
accelerate ulcer healing or to prevent the
recurrent ulcers in NSAID users. Our studies in
almost 6,000 dyspeptic patients
undergoing upper endoscopy and [(13)C]-urea
breath test (UBT) revealed that about 70%
of these patients are H. pylori (+) and about 30.6%
of these develop gastroduodenal ulcers.
Of these ulcers, over 70% were H. pylori (+)
positive, 12% NSAID (+), 8% were both H. pylori
(+) and NSAID (+), while 22% ulcers were H.
pylori (-) and NSAID (-) or "idiopathic"
ulcers. Basically, our results support Hawkey's
concept and this also agrees with our findings in
the rat model showing that: (1) there is
no synergistic interaction between H. pylori
infection and NSAID on gastric ulcer development,
(2) H. pylori and NSAID are independent risk
factors for peptic ulceration, and (3) NSAID
therapy in H. pylori positive patients attenuates
the ulcer development possibly due to direct
inhibitory action of these drugs on H. pylori. |
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Clinical science of
Helicobacter pylori infection: ulcers and
NSAIDs. |
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Br Med Bull
1998;54(1):55-62 (ISSN: 0007-1420) |
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Calam J |
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Division of
Medicine, Imperial College School of Medicine,
Hammersmith Hospital, London, UK. |
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It
is now clear that Helicobacter pylori
is a major aetiological factor in peptic ulcer
disease. About 95% of patients with
duodenal ulcers and perhaps 80%
of patients with gastric ulcers are
infected with this bacterium and its eradication
greatly diminishes recurrence of these ulcers.
Many patients are still not receiving the benefit
of this treatment, however. Most patients who
have peptic ulcers without H. pylori infection
are taking non-steroidal anti-inflammatory drugs
(NSAIDs), although this may not
be recognised or admitted. Such patients have to
be managed by withdrawal of these agents or by
giving protective agents such as misoprostol. If
H. pylori is present in a patient who develops an
ulcer whilst taking NSAIDs, it remains unclear
whether it is beneficial to eradicate the
infection, but this seems advisable in case the
ulcer is due to the infection in that particular
patient. |
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| obere GIT-Blutung /
blutende
Ulcera sowie
Helicobacter bezw. NSAR |
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Interaction
between Helicobacter pylori and non-steroidal
anti-inflammatory drugs in peptic ulcer bleeding.
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Scand J
Gastroenterol 1999 Mar;34(3):234-7 (ISSN: 0036-5521) |
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Wu CY; Poon SK;
Chen GH; Chang CS; Yeh HZ |
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Dept. of
Internal Medicine, Taichung Veterans General
Hospital, Taiwan. |
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BACKGROUND:
Helicobacter pylori and non-steroidal anti-inflammatory
drugs (NSAIDs) are the two primary causes of
peptic ulcer disease. How H. pylori and NSAIDs
interact and influence the development of ulcer
bleeding is still not clear. METHODS: A hospital-based,
age- and sex-matched case-control study was
conducted. Multivariate and stratified analyses
were performed for further evaluation of the
interaction between H. pylori and NSAIDs. RESULTS:
Ninety-seven patients (52 gastric ulcers, 45
duodenal ulcers) and 97 non-ulcer controls were
enrolled in the study. H. pylori and
NSAIDs were both found to be independent risk
factors for ulcer bleeding (H. pylori
odds ratio, 2.22; 95% confidence interval (CI), 1.23-4.01;
NSAIDs odds ratio, 4.57; 95% CI, 2.50-8.35). There
was no synergistic effect. In contrast, a
negative interaction was observed in the
logistic regression and stratified analysis,
although the difference was not significant (H.
pylori adjusted odds ratio, 3.47; 95% CI, 1.73-6.95;
NSAID adjusted odds ratio, 6.16; 95% CI, 3.14-12.09).
CONCLUSION: H. pylori increases the risk of
peptic ulcer bleeding but may play a protective
role in NSAID users. |
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Comment In:
Comment In: RefSourcd:Scand J Gastroenterol. 1999
Mar; 34(3):225-8/PMID:10232863 |
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Non-steroidal anti-inflammatory
drugs, Helicobacter pylori and bleeding
gastric ulcer. |
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Aliment
Pharmacol Ther 2000 Feb;14(2):203-9 (ISSN: 0269-2813) |
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Ng TM; Fock KM;
Khor JL; Teo EK; Sim CS; Tan AL; Machin D |
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Division of
Gastroenterology, Department of Medicine, Changi
General Hospital, Singapore. |
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BACKGROUND:
Helicobacter pylori infection and NSAID usage are
considered to be independent risk factors for
gastric ulcer (GU). Whether they interact to
influence the risk of bleeding in GU is unclear.
AIM: To determine the prevalence of H. pylori
infection and NSAID ingestion in a group of
patients with GU and determine their roles in
bleeding and non-bleeding GU. METHODS AND RESULTS:
From January 1993 to June 1996, a total of 217 GU
patients (150 male, 67 female, median age 61
years, range 26-94) were eligible for the study.
Eighty-five per cent were H. pylori-positive and
15% were H. pylori-negative. NSAID usage within 4
weeks prior to endoscopy was present in 30%, more
in the H. pylori-negative than H. pylori-positive
patients (59% vs. 25% P = 0.0002). Aspirin was
most commonly used (43%). One hundred patients
bled from GU (69 male, 31 female, mean age 67
years, range 26-94) and 117 did not (81 male, 36
female, mean age 57 years, range 28-86).
Univariate logistic regression showed that
advanced age (>/= 65 years) and NSAID usage
carried an increased risk of bleeding GU (odds
ratio 3.4 and 6.8, respectively) while H. pylori
infection alone was not associated with
additional risk (OR = 0.8). However, when three
variables were considered jointly in a multiple
logistic regression, the OR associated with H.
pylori infection increased to 2.4, suggesting
that in the presence of NSAIDs and advanced age,
H. pylori also increases the risk of bleeding GU,
indicating an interaction between the variables.
CONCLUSION: NSAID usage and advanced age
are risk factors for bleeding GU, whereas H.
pylori infection by itself is not. In
the presence of NSAIDs and advanced age, an
increased risk of bleeding GU with H. pylori is
observed, indicating the possibility of an
interaction between these factors. |
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Helicobacter pylori
and risk of ulcer bleeding among users of
nonsteroidal anti-inflammatory drugs: a case-control
study. |
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Gastroenterology
1999 Jun;116(6):1305-9 (ISSN: 0016-5085) |
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Aalykke C;
Lauritsen JM; Hallas J; Reinholdt S; Krogfelt K;
Lauritsen K |
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Department of
Medical Gastroenterology, Denmark. Aalykke@med.ou.dk. |
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BACKGROUND
& AIMS: Peptic ulcer complications related to
use of nonsteroidal anti-inflammatory drugs (NSAIDs)
are among the most common serious adverse drug
reactions. Whether Helicobacter pylori infection
potentiates this gastrointestinal toxicity of
NSAIDs is still unresolved. In this study, we
investigated the role of H. pylori as a cause of
bleeding peptic ulcer among NSAID users. METHODS:
A case-control study of current users (n = 132)
of NSAIDs (including acetylsalicylic acid),
admitted because of bleeding peptic ulcer, was
performed. Controls were 136 NSAID users without
gastrointestinal complications. H. pylori was
diagnosed by either increased levels of serum
immunoglobulin G or by 13C-urea breath test.
RESULTS: Fifty-eight (44%) case subjects had a
bleeding gastric ulcer, 54 (41%) had a bleeding
duodenal ulcer, 12 (9%) had both gastric and
duodenal ulcers, and 8 (6%) had hemorrhagic
gastritis. H. pylori was present in 75 (57%)
cases compared with 59 (43%) controls.
The adjusted odds ratio of bleeding peptic ulcer
among NSAID users associated with H. pylori
infection was 1.81 (95% confidence interval, 1.02-3.21).
H. pylori accounted for approximately 24% of
bleeding peptic ulcers among elderly NSAID users.
CONCLUSIONS: NSAID users infected with H.
pylori have an almost twofold increased risk of
bleeding peptic ulcer compared with NSAID users
without H. pylori. |
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Comment
In: Comment In: RefSourcd:Gastroenterology. 2000
Feb; 118(2):451-2/PMID:10691374 |
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Relationship between
non-steroidal anti-inflammatory drug use and
Helicobacter pylori infection in bleeding or
uncomplicated peptic ulcers: A case-control study.
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J
Gastroenterol Hepatol 2003 Jan;18(1):18-25 (ISSN:
0815-9319) |
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Okan
A; Tankurt E; Aslan BU; Akpinar H; Simsek I;
Gonen O |
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Departments
of Gastroenterology and Public Health, Dokuz
Eylul University Medical School, Inciralti-Izmir,
Turkey. abokan@superonline.com. |
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BACKGROUND AND AIMS: Non-steroidal
anti-inflammatory drug (NSAID) use has been
closely associated with an increased risk of
bleeding peptic ulcers, while the prevalence of
Helicobacter pylori infection has been reported
to be lower in bleeding ulcers than in non-bleeding
ones. However, whether an interaction exists
between NSAID use and H. pylori infection has not
clearly been elucidated yet. The aims of this
study were to determine the frequency of NSAID
use and H. pylori infection, to predict risk
factors in bleeding peptic ulcers and to
determine whether NSAID use and H. pylori
infection interact with each other. METHODS:
Ninety-six patients with bleeding ulcer were
included in the study. The control group
consisted of 106 patients with non-bleeding ulcer.
Data were analyzed by using the chi-squared test,
Fisher's exact test and logistic regression
analysis with or without interaction term (H.
pylori by NSAID). RESULTS: Non-steroidal anti-inflammatory
drug use was significantly more common in
patients with bleeding ulcers than in controls (79.2
vs 38.7%, unadjusted odds ratio (OR): 6.02, 95%
confidence interval (CI): 3.21-11.29). The
frequency of the H. pylori infection was
significantly lower in patients with bleeding
ulcers than in controls (66.7 vs 89.6%,
unadjusted OR: 0.23, 95% CI: 0.10-0.49). In the
logistic regression analysis with the interaction
term, male sex (adjusted OR: 3.70, 95% CI: 1.65-8.29),
multiplicity of ulcers (adjusted OR: 4.10, 95% CI:
1.02-16.45) and NSAID use (adjusted OR: 33.87, 95%
CI: 4.36-262.97) were independent risk factors
for bleeding ulcers. There was a negative
interaction between H. pylori and NSAID use (adjusted
OR: 0.09, 95% CI: 0.01-0.83). CONCLUSIONS:
The negative interaction between the two
variables suggests that the presence of H. pylori
is associated with a lower risk of bleeding in
ulcer patients taking NSAIDs. [Copyright
2003 Blackwell Publishing Asia Pty Ltd]. |
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| obere GIT-Blutung /
blutende
Ulcera und NSAR |
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- ohne
Helicobacter Pylori |
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Risk of upper
gastrointestinal bleeding associated with non-aspirin
cardiovascular drugs, analgesics and nonsteroidal
anti-inflammatory drugs. |
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Eur J
Gastroenterol Hepatol 2003 Feb;15(2):173-8 (ISSN:
0954-691X) |
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Lanas
A; Serrano P; Bajador E; Fuentes J; Sainz R |
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Service of
Gastroenterology, University Hospital Lozano
Blesa, C/San Juan Bosco 15, 50009 Zaragoza, Spain.
alanas@posta.unizar.es |
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OBJECTIVE:
To evaluate the risk of upper gastrointestinal
bleeding associated with non-aspirin
cardiovascular drug therapy, common analgesics
and individual nonsteroidal anti-inflammatory
drugs (NSAIDs).
METHODS: The case group was made up of 1122
consecutive patients admitted with bleeding from
a peptic lesion. The 2231 control subjects
consisted of 1109 patients hospitalized for other
reasons and 1122 outpatients from the same
geographical area. The relative risk was
calculated by unconditional logistic regression
after adjusting for confounding factors.
RESULTS: The use of the antiplatelet agent
triflusal, and other commonly used cardiovascular
drugs, such as beta-receptor blockers and calcium
channel blockers, was not associated with
increased risk of upper gastrointestinal bleeding.
The use of angiotensin-converting enzyme
inhibitors reduced the risk of bleeding by 30% (odds
ratio 0.7; 95% confidence interval 0.5-0.96). Use
of ketorolac (odds ratio 59.4;
95% confidence interval 7.7-454) and piroxicam
(odds ratio 19.6; 95% confidence interval 9.3-35.3)
carried the highest risk. Use of paracetamol and
tramadol was not associated with increased risk
of bleeding, but the non-narcotic agent metamizol
was associated with a small increase in risk of
upper gastrointestinal bleeding (odds ratio 2.6;
95% confidence interval 1.3-5.2).
CONCLUSIONS: The use of the antiplatelet agent
triflusal and other cardiovascular drugs apart
from low-dose aspirin was not associated with
gastrointestinal bleeding. The use of either
NSAIDs or aspirin increased the risk of
gastrointestinal bleeding but, among the
analgesics, only metamizol induced a small
increase in the risk of gastrointestinal bleeding.
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Upper gastrointestina
l bleeding among users of NSAIDs: a population-based
cohort study in Denmark. |
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Br
J Clin Pharmacol 2002 Feb;53(2):173-81 (ISSN:
0306-5251) |
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Mellemkjaer L;
Blot WJ; Sorensen HT; Thomassen L; McLaughlin JK;
Nielsen GL; Olsen JH |
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Institute of
Cancer Epidemiology, Danish Cancer Society,
Strandboulevarden 49, DK-2100 Copenhagen O,
Denmark. lene@cancer.dk. |
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AIMS:
It is well-known that use of nonsteroidal anti-inflammatory
drugs (NSAIDs) increases the risk of upper
gastrointestinal bleeding (UGIB), but
characteristics of the association and
quantification of excess risk at the population
level require clarification.
METHODS: All users of nonaspirin prescription
NSAIDs in North Jutland County, Denmark during
1991-95 were identified in the regional Pharmaco-Epidemiologic
Database. Using the Hospital Discharge Register,
all hospitalizations for UGIBs were identified
among the 156,138 users of NSAIDs and compared
with the number of expected based on the North
Jutland population who did not receive NSAID
prescriptions.
RESULTS: During periods of NSAID use without use
of other drugs associated with UGIB, we observed
365 UGIBs, a number 3.6 times higher than
expected (95% CI = 3.3, 4.0). The excess
risk varied by sex, type of NSAID and form and
route of administration of the NSAID, but not by
age at first NSAID prescription or number of
prior prescriptions. Risk declined sharply
following cessation of use. For ibuprofen and
naproxen, there was a clear trend in rising risk
by increasing dose, although the lowest doses
were also associated with an excess of UGIB.
Concurrent use of corticosteroids, anticoagulants
and aspirin further increased the risk of UGIB.
CONCLUSIONS: All types and formulations of NSAIDs
appear to increase the risk of UGIBs, but the
effect appear not to be cumulative and diminish
rapidly with discontinue of use. Up to 15% of the
UGIBs in the entire population of the North
Jutland County may be explained by use of this
drug. |
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