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Sunday, June 26, 2016

Most Common Diseases of 50 Plus - Upper gastrointestinal disorders: Gastric Ulcers- The Causes and Risk factors

Kyle J. Norton(Scholar, Master of Nutrients), all right reserved.
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bio science, ISSN 0975-6299.

           Upper gastrointestinal (GI) diseases

The prevalence of upper gastrointestinal (GI) diseases is increasing in subjects aged 65 years and over. Pathophysiological changes in esophageal functions that occur with aging may, at least in part, be responsible for the high prevalence of
1. Gastro-esophageal reflux disease (GERD) in old age.

2. The incidence of gastric and duodenal ulcers and their bleeding complications is increasing in old-aged populations worldwide.

3. H. pylori infection in elderly patients with H. pylori-associated peptic ulcer disease and severe chronic gastritis.

4. Almost 40% of GU and 25% of DU in the elderly patients are associated with the use of NSAID(1) and/or aspirin(2).(a)

                           Gastric ulcers

Gastric ulcer, a type of peptic ulcer is defined as a condition of a localized tissue erosion in the lining the stomach.

              The Causes and Risk factors 

The 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.

The 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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