1. Congenital causes
There is a report of seven cases of congenital anomalies in adults, duodenal obstruction and peptic ulcer disease developed. There were two cases of congenital duodenal web, two of hypertrophic pyloric stenosis, two of annular pancreas,according to the study by Dr. Naylor RG and Dr. Juler GL Fortunately, treatment should be directed toward relief of the duodenal obstruction and the reduction of basal acid secretion by truncal vagotomy in all such cases(4).
In the study of the causes of the incompetence of stump sutures in resection of the stomach observed in 90 out of 3479 patients with chronic duodenal ulcers, showed that most patients have a combination of general and local factors. Among the local factors the leading one was appearance of a large inflammatory infiltration around the “active” ulcers(5).
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.(6).
4. 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(7). 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(8).
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