Abstract
Many etiological hypotheses have been suggested to explain the development of peptic ulcers during the last 300 years (including gastric ulcer and duodenal ulcer). In the last two decades, significant progress has been made in understanding the pathophysiology of peptic ulcer disease, particularly with regard to the involvement of Helicobacter pylori and nonsteroidal anti-inflammatory medications (NSAIDs). This study will attempt to review literature on etiology and management of gastric and duodenal ulcers among adolescents.
Highlights
Ulcers are included in the term peptic ulcer disease (PUC)
*Corresponding author: E-mail: elshmaa3332004@yahoo.com; Aladainan et al.; JPRI, 33(37B): 289-297, 2021; Article no.JPRI.71179 and infection with Helicobacter pylori bacteria are some of the factors that may lead to ulcer development
In the last two decades, significant progress has been made in understanding the pathophysiology of peptic ulcer disease, with regard to the involvement of Helicobacter pylori and nonsteroidal anti-inflammatory medications (NSAIDs)
Summary
Ulcers are included in the term peptic ulcer disease (PUC). Reduced efficiency of the Many individuals have ulceration of the gastric or stomach mucosal barriers, excessive acid output, duodenal mucosa. Physician-diagnosed PUD had a 1-year frequency of 0.12–1.%, while PUD diagnosed during hospitalizations had a 1-year prevalence of 0.10–0.19% [4] Their results demonstrate that the prevalence of PUD has reduced in many nations in recent decades, most likely due to a reduction in H. pylori infection, especially in Western populations [4]. When compared to the lower rates found in other studies of physician-diagnosed PUD in primary care, it appears that a proportion of people with PUD go undetected. Severe consequences, such as gastrointestinal bleeding, may be the initial signs of PUD in people who are asymptomatic. Over this time period, prescriptions for medicines implicated in the aetiology of PUD, such as aspirin and NSAIDs, have increased, and adherence to gastroprotection for the prevention of NSAIDinduced PUD remains far from optimum [9]
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