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Microbes & Immunity Peptic ulcer disease among adolescent girls

Increased psychological stress levels, frequently worsened A polygenic inheritance pattern and genetic
by socioeconomic burden, may contribute to the onset and predisposition to PUD may contribute to the disease’s
aggravation of PUD among Africans. Prolonged stress can familial aggregation. Duodenal and stomach ulcers have
alter the integrity of the mucosa and release of stomach different patterns of familial aggregation, with first-degree
acids, making individuals more susceptible to ulcers. relatives of patients exhibiting a higher prevalence of
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In many African nations, tobacco use is a common habit ulcers. For example, duodenal ulcers are associated with
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linked to an increased risk of PUD. Dietary factors that host polymorphism affecting cytokine IL-1β levels. In a
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can irritate the stomach mucosa and contribute to PUD previous meta-analysis, Zhang et al. conducted subgroup
development include the consumption of spicy foods analyses of data from 3,793 participants and revealed that
and large amounts of alcohol, irregular eating patterns, the IL-1β–31 C/C genotype has a protective effect against
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inadequate nourishment, and poor food choices. 22 the development of duodenal ulcers. However, in the same
study, no evidence of a significant correlation was observed
Cigarette smoking is considered one of the main causes
of the development of ulcers. Hazardous duodenal contents between the IL-1β–31 C/T polymorphism and duodenal
ulcers; thus, it remains unclear whether duodenal ulcers
can reflux back into the stomach as a result of cigarette are caused by H. pylori infection. 25
smoking. Moreover, there seems to be a greater risk of
H. pylori infection among smokers. This elevated risk 3.2. Understanding PUD occurring in adolescent
could be attributed to the detrimental effects of smoking girls across Africa
on the antioxidant levels or immune system, which is
locally present in the mucosa of the gastroduodenum. In adolescent girls, PUD can present with various clinical
These activities have the potential to compromise the manifestations. Abdominal pain is one of the most
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natural defenses of the stomach and duodenum against prevalent symptoms of peptic ulcers in children. Other
symptoms may include vomiting, melena, nausea, stomach
H. pylori. The innermost layer of epithelium forms a discomfort, hematemesis, abdominal distension, sour
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continuous layer of defense against harmful substances regurgitation, ozostomia, eructation, paleness, bloody
in the lumen. A detrimental impact of smoking cigarettes 26
is the stimulation of cell apoptosis, which causes tissue feces, poor appetite, and abdominal tenderness. The signs
and symptoms of PUD vary depending on the disease
damage and gastrointestinal tract malfunction. 23
location and patient’s age. Gastric and duodenal ulcers can
Urease, which converts urea into ammonia and carbon be distinguished by the timing of symptom occurrence
dioxide to neutralize the acidic pH and shield bacterial cells (before or after meals). Nocturnal pain is frequently
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from stomach acids, is essential for H. pylori colonization. observed in cases of duodenal ulcers. Patients with gastric
H. pylori can weaken the mucus gel layer and decrease outlet obstruction may report abdominal bloating and/
prostaglandin synthesis, which makes it easier for irritants or fullness. Warning or alarm symptoms that should
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such as pepsin and gastric acid to enter deeper into the necessitate immediate referral include unintentional
stomach wall layers and cause mucosal damage and weight loss, progressive dysphagia, overt gastrointestinal
ulcer development. Peptic ulcers may occur as a result bleeding, iron deficiency anemia, recurrent emesis, and
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of a dysregulation in the equilibrium between aggressive family history of upper gastrointestinal malignancies. 28,29
agents and defense mechanisms in the duodenum and Table A1 shows the symptoms of PUD among adolescent
stomach. Histologically, chronic peptic ulcers exhibit girls in Africa, as reported in studies published between
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well-defined ulcer bases, granulation tissue formation, 2013 and 2024.
fibrosis, and scarring in deeper layers, whereas acute peptic
ulcers may exhibit surface erosions, fibrinoid necrosis, and 3.3. Prevalence and incidence of PUD
inflammatory cell infiltrates. Hematemesis and melena, PUD is a common affliction worldwide. Over 300,000
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perforation leading to peritonitis, and blockage from global deaths were attributed to PUD in 2013, according to
scarring and fibrosis are certain complications associated estimates from the Global Burden of Disease. A previous
5
with peptic ulcers. Peptic ulcers heal through a combination study conducted in northern Sudan reported a prevalence
of mechanisms, including angiogenesis, tissue repair, of H. pylori infection of 8.4% among adolescents aged
inflammation resolution, and mucosal regeneration. Ulcer 10 – 18 years. In addition, a study conducted in Egypt
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recurrence is caused by various factors, such as NSAID demonstrated that 407 (64.6%) adolescents aged ≤18 years
use, defective tissue repair, persistent H. pylori infection, tested positive for H. pylori, with the highest prevalence
and systemic diseases. Figure A1 shows the pathogenesis of H. pylori infection reported among adolescents aged
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of PUD, which involves both aggressive and defensive >10 years (32.9%). In another study conducted in
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factors. Owerri, Nigeria, the prevalence of H. pylori infection was

Volume 1 Issue 2 (2024) 5 doi: 10.36922/mi.3078