Gastric ulcers
Gastric ulcer, a type of peptic ulcer is defined as a condition of a localized tissue erosion in the lining the stomach.
Causes and Risk factors
B.1. Causes
1. Imbalance between stomach acid and upper GI tract mucosa
Imbalance between stomach acid is the lead cause of Gastric ulcer is
caused by the imbalance between stomach acid and upper GI tract mucosa.
Acid-related disorders are common conditions that negatively impact
quality of life for a significant number of people nationwide. The
pathology of these conditions involves an imbalance between acid
secretion by gastric parietal cells and the ability of upper GI tract
mucosa to defend against the effects of the acid(7).
2. Medication
Medication such as aapirin and Non-steroidal anti-inflammatory drugs
(NSAIDs) may adversely cause damage throughout the gastrointestinal
tract and aggravate pre-existing disease. OTC NSAIDs should be taken on a
fasting stomach, not with food as commonly advocated. Epidemiological
studies show an association between NSAID intake and serious events.
Ibuprofen is consistently at the lower end of toxicity rankings, whereas
ketorolac and azapropazone are the worst. The risk of bleeding is
increased with advancing age, presence of HP, previous history of
bleeding, anticoagulant use, etc.(9).
3. Helicobacter pylori and chronic gastritis
Helicobacter pylori is a Gram-negative, microaerophilic bacterium found
in the stomach. In developed countries, the prevalence of this
infection has decreased, although it continues to be high. The
prevalence in Spain is high (50%) and does not seem to be decreasing.
There is an increase in antibiotic resistance, which is correlated with
the frequency of prior antibiotic prescription. H. pylori eradication
improves the symptoms of “epigastric pain syndrome” in functional
dyspepsia. The frequency of idiopathic peptic ulcers seems to be
increasing(10). Other study indicated that the GU series differed from
the controls in having a higher degree of HP colonisation in gastric
mucosa. The relative risks (RR) in predicting high GU connected with
high HP colonisation were significantly elevated, both in the antrum (RR
= 6.0-4.8) and in the corpus (RR 5.0-4.4), and still higher when
combined HP colonisation values were used (RR 9.5-7.1). The persistence
of active ulcer (GU+) was associated with a very high level of HP
colonisation, with absence of corpus atrophic gastritis at the first
examination and with young patients. The presence of HP infection as
well as the level of HP colonisation are of importance in both the
development and chronicity of peptic GU disease(11).
4. Etc.
B.2. Risk factors
1. Periodontal disease
In the analyzed study of the eligible 28 765 subjects, peptic ulcer was
present in 397 (1.4%). The results of bivariate analyses showed that a
significantly higher proportion of subjects with peptic ulcer reported
that they lost five or more teeth (35.3 vs. 17.4%, p<0.001) or
that they were told they had periodontitis (33.5 vs. 20.7%,
p<0.001)(8).
2. Aging
In the study by Osaka City University Graduate School of Medicine,
indicated that he total number of elderly persons with gastric ulcers in
Japan is increasing with an improvement in the average life expectancy.
So far, gastric ulcer in elderly persons is considered proximal gastric
ulcer due to corpus-predominant atrophic gastritis(12).
3. Smoking
In the study by University of Hong Kong found that cigarette smoking
increases xanthine oxidase activity, leukotrienes, and nitric oxide
production and also neutrophil infiltration in the gastric mucosa. On
the other hand, it reduces blood flow, prostaglandin production,
epithelial cell proliferation, and formation of blood vessels in the
tissue(13).
4. Mechanical ventilation
Mechanical ventilation increases risk for bleeding in the upper part of
the gastrointestinal tract. In the study to compare the effectiveness of
famotidine (a histamine(2) antagonist) and pantoprazole (a proton pump
inhibitor) in preventing stress ulcers in critically ill patients
receiving mechanical ventilation, showed that in a total of 522 patients
who received famotidine and 95 who received pantoprazole were included.
Bleeding in the upper part of the gastrointestinal tract was more
common in patients receiving pantoprazole than in patients receiving
famotidine (0.38% vs 3.2%, P= .03)(14).
5. Critical illness
Critical illness such as ischemia can lead to back-diffusion of H+ ions
through increased membrane permeability. Impaired mucosal buffering then
leads to intramural acidosis and cell death(15).
8. Etc.
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Sources
(7) http://www.ncbi.nlm.nih.gov/pubmed/11729446.
(8) http://www.ncbi.nlm.nih.gov/pubmed/22980150
(9) http://www.ncbi.nlm.nih.gov/pubmed/23163547
(10) http://www.ncbi.nlm.nih.gov/pubmed/23018004.
(11) http://www.ncbi.nlm.nih.gov/pubmed/1759132
(12) http://www.ncbi.nlm.nih.gov/pubmed/21061517
(13) http://www.ncbi.nlm.nih.gov/pubmed/9872502
(14) http://www.ncbi.nlm.nih.gov/pubmed/18310651
(15) http://www.ncbi.nlm.nih.gov/pubmed/7495942
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