UEG Journal Abstracts 2023 - 707

Mean MCV of the study patients was estimated and compared between
groups. The mean MCV was found 85.45±6.93 (on fL) in group A and
88.73±4.58 (on fL) in group B. The difference was found to be statistically
significant between the two groups (p=0.001).
Mean MCH of the study patients was estimated .The mean MCH was found
27.6±2.4 pg in group A and 28.8±1.4 pg in group B. The difference was
found to be statistically significnat (p<0.05).
S. ferritin >39 ug/L was found in 91 % group A, 67.9% of group B and
<15ug/L was found in 18% of group A and 13..4% in group B subjects. This
difference is statistically significant.
In male patients frequency of depleted/low iron stores anemia was 2 in
low hemoglobin level in Group A but none was in Group B. Adequate iron
store was found in 8 and 5 patients in group A and group B respectively.
The differences was not statistically significant (p>0.05).
In male patients frequency of depleted/low iron stores was 12 in normal
hemoglobin level in Group A. In Group B depleted/low iron stores was
found in 2 patients with normal hemoglobin level. Adequate iron store
was found in 40 and 36 patients in group A and group B respectively. The
difference was statistically significant (p<0.05)
In female patients frequency of depleted/low iron stores anemia was 8 in
low hemoglobin level in Group A but none was found in Group B. Adequate
iron store was found in 7 and 1 patients in group A and group B respectively.
The difference was not statistically significant (p>0.05).
Frequency of depleted/low iron stores anemia was 27 in patients with normal
hemoglobin level in Group A and 2 in Group. Adequate iron store was
found in total 63 and 45 patients in group A and group B respectively. The
difference was statistically significant (p<0.05).
Conclusion: This study revealed an association of iron deficiency anaemia,
low serum ferritin , low MCH and MCV with H.pylori infection. So there
is a possibility of causal relation between H. Pylori infection and iron deficiency
anaemia.
References: To be provided if the abstract is accepted or earlier on request.
Disclosure: Nothing to disclose.
PP0331
RELATIONSHIP BETWEEN HELICOBACTER PYLORI INFECTION AND
GASTRIC MUCOSAL INJURIES IN PATIENTS TAKING ASPIRIN
Y. Shimada1
A. Murata1, S. Sato1, A. Nagahara2
1
, Y. Terai1, R. Om1, Y. Kita1, Y. Ikeda1
, T. Genda1
, S. Sato1
,
Juntendo University Shizuoka Hospital, Gastroenterology and
Hepatology, Izunokuni-city, Japan, 2
Medicine, Gastroenterology, Tokyo, Japan
Juntendo University School of
Contact E-Mail Address: yshimada@juntendo.ac.jp
Introduction: The mechanism of aspirin-induced gastric mucosal injury is
thought to be mediated by multiple processes involving either topical or
systemic effects. Recently, it has been reported that topical effects play a
pivotal role in causing gastric mucosal injury 1, 2
.
It is known that almost all aspirin-induced gastric mucosal injuries were
observed in low intragastic pH condition (pH<4) 3
.
Though it depends on the severity and distribution of gastritis caused by
Helicobacter pylori (H. pylori), gastric acid secretion is recovered after the
eradication of H. pylori 4
.
Therefore, because intragastric pH may decrease dramatically, the prevalence
and severity of gastric mucosal injuries in patients taking aspirin
may also change after the eradication.
Aims & Methods: The aim of this study is to reveal the relationship between
H. pylori infection and gastric mucosal injuries in patients taking
aspirin. This study was a retrospective cross-sectional study. Data were extracted
from the records of subjects who underwent upper gastrointestiVol.
11 | October 2023
707
nal endoscopy at our department between April 2015 and March 2020. We
focused on the subjects taking only aspirin as an anti-thrombotic agent,
and selected the subjects whose H. pylori infection status was known.
After that we divided into three groups (non-infection, current infection,
and past infection of H. pylori) and compared the severity of gastric mucosal
injury, individually. Severity of gastric mucosal injury was evaluated
endoscopically based on the modified LANZA score (m-LANZA score). Statistical
analyses were performed by using Fisher's exact test.
We evaluated separately for subjects with concomitant use of potassiumcompetitive
acid blocker (P-CAB) or PPI (user) and subjects without concomitant
use of P-CAB, PPI nor histamine H2 receptor antagonist (H2RA)
(nonuser).
Results: 311 subjects out of 6,031 were taking only aspirin as an antithrombotic
agent. In group of non-infection (43 men, 32 women; mean
age 69.0±15.6 years), average MLS was 0.51±1.16 (user: n=45, score0=33,
score1=8, score2=1, score3=1, score4=0, score5=2) and 1.21±1.70 (nonuser:
n=29, score0=18, score1=0, score2=3, score3=5, score4=1, score5=2). In
group of current infection (12 men, 5 women; mean age 67.7±11.4 years),
average MLS was 0.86±1.86 (user: n=7, score0=5, score1=1, score2=0,
score3=0, score4=0, score5=1) and 1.29±1.89 (nonuser: n=7, score0=4,
score1=0, score2=2, score3=0, score4=0, score5=1). In group of past infection
(107 men, 51 women; mean age 74.7±7.5 years), average MLS
was 0.39±1.07 (user: n=104, score0=86, score1=8, score2=4, score3=2,
score4=1, score5=3) and 0.90±1.62 (nonuser: n=49, score0=34, score1=4,
score2=3, score3=4, score4=2, score5=4).
There was a statistically significantly difference between user and nonuser
in group of non-infection (p=0.040) and in group of past infection
(p=0.023). Mean MLS in group of current infection was high more than expected
because intragastric pH might be high in H. pylori-positive patients.
We considered because many subjects which were H. pylori-positive but
whose gastric acid secretion was not so impaired might be included in this
study.
Conclusion: There was no significant difference between H. pylori infection
and gastric mucosal injuries in patients taking low dose aspirin. However,
concomitant use of P-CAB or PPI can prevent gastric mucosal injuries
in pylori-negative patients taking low dose aspirin.
References:
1. Musumba C, et al. Review article: cellular molecular mechanisms of
NSAID-induced peptic ulcers. Aliment Pharmacol Ther. 30:517-531 2009
2. Mashita Y, et al. Oral but parenteral aspirin upregulates COX-2 expression
in rat stomachs. a relationship between COX-2 expression and PG deficiency.
Digestion. 73:124-132 2006
3. Nishino M, et al. Relationship between low-dose aspirin-induced gastric
mucosal injury and intragastric pH in healthy volunteers. Dig Dis Sci.
55:1627-1636, 2010
4. El-Omar EM, et al. Helicobacter pylori infection and chronic gastric hyposecretion.
Gastroenterology. 113:15-24 1997
Disclosure: Nothing to disclose.
H. pylori
UEG Journal Abstracts 2023

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