Analysis of clinical feature differences and influencing factors between children with peptic ulcer and healthy children

Peptic ulcers are often thought of as an adult ailment, but a new study from a tertiary hospital in Xiamen, China, is drawing attention to how frequently they strike children — and how many of the risk factors are modifiable. Researchers led by Caiyan Chen and Huiying Qiu of Zhongshan Hospital of Xiamen University conducted a retrospective case-control analysis of 92 children aged 8 to 14 years diagnosed with gastric or duodenal ulcers by gastroscopy, comparing them with 92 healthy children examined during the same period. Their findings, published in Frontiers in Pediatrics, identify five independent risk factors for pediatric peptic ulcer: Helicobacter pylori infection, a high-sugar diet, a family history of digestive system diseases, boarding school attendance, and psychological disorders. The strongest of these was psychological disorder, with an odds ratio of 6.11, followed by H. pylori infection at 4.23.

The clinical picture in the ulcer group was strikingly different from that of the healthy controls. Abdominal pain was reported in 82.6 percent of children with ulcers versus 15.2 percent of healthy children, vomiting in 63.0 percent versus 8.7 percent, and melena — black, tarry stools indicating gastrointestinal bleeding — in 19.6 percent versus zero percent. Laboratory indicators reinforced the divide: H. pylori infection, detected by the 13C-urea breath test, was present in 63.0 percent of the ulcer group versus 8.7 percent of controls, and anemia affected 45.7 percent versus 12.0 percent. A positive fecal occult blood test was found in 38.0 percent of children with ulcers compared with just 3.3 percent of healthy children. Gastroscopy revealed that ulcers predominantly occurred in the duodenal bulb, accounting for 68.5 percent of cases, followed by the gastric antrum at 23.9 percent and compound ulcers affecting both stomach and duodenum at 7.6 percent.

Why does the duodenal bulb emerge as the most vulnerable site? The researchers point to its distinctive anatomy and physiology. The duodenal bulb mucosa lacks the protective mucus layer found elsewhere in the gastrointestinal tract, and its submucosa is richly supplied with blood vessels and nerve endings, making it susceptible to acid erosion. This site sits in the peak area of gastric acid secretion, and gastric antrum motility can directly transport acid toward the duodenal bulb, creating a locally high-acid environment. The gastric antrum, the second most common ulcer location, may be vulnerable because of H. pylori colonization patterns, antral motility, and relatively weak local mucosal defense. The presence of compound ulcers in a subset of children suggests that multi-site involvement can occur, underscoring the need for comprehensive endoscopic examination rather than targeted inspection of a single region.

The mechanism behind abdominal pain in these children is closely tied to ulcer location and inflammatory mediators. The duodenal bulb submucosa contains a rich supply of nerve endings, and once an ulcer forms, it directly stimulates pain-sensing fibers, triggering upper abdominal or periumbilical pain. Mediators such as prostaglandins and histamine released during the inflammatory response around the ulcer enhance nerve sensitivity and lower the pain threshold. Notably, the abdominal pain in the ulcer group was mainly postprandial — occurring after meals — which the researchers attribute to the peak period of gastric acid secretion and increased gastric antrum motility. After eating, acid that is not neutralized by food contacts the ulcer surface directly, exacerbating pain, while increased antral motility may push acid toward the duodenal bulb, aggravating local irritation. In contrast, the low incidence of abdominal pain among healthy children was mostly functional, related to motility abnormalities or visceral hypersensitivity rather than organic lesions.

Vomiting and melena reflect the complication profile of peptic ulcers. The significantly elevated vomiting rate in the ulcer group may be related to pyloric obstruction or delayed gastric emptying: when an ulcer is located near the pylorus, local edema or scar formation can cause mechanical stenosis, producing postprandial vomiting that may contain bile. Vagus nerve excitation caused by the ulcer can also inhibit gastric antrum motility and delay emptying, leading to nausea and vomiting. Melena, a typical manifestation of gastrointestinal bleeding, arises when ulcer erosion damages blood vessels. In children, bleeding often presents as occult blood loss or small amounts of hematemesis, partly because children have thinner blood vessels and bleeding is prone to self-coagulation. However, long-term chronic blood loss can lead to anemia — which explains the markedly higher anemia incidence in the ulcer group. The complete absence of melena in the healthy group further confirms its clinical value as a specific symptom of peptic ulcer.

H. pylori infection remains a core risk factor, and its pathogenic mechanism is well validated. The bacterium participates in ulcer formation through multiple pathways: damaging the gastric mucosal barrier, promoting inflammatory responses, and affecting gastric acid secretion. Its urease decomposes urea to produce ammonia, directly damaging epithelial cells; the cytotoxin-associated gene protein it releases induces epithelial cell apoptosis; and cytokines released during inflammation activate immune cells, creating a chronic inflammatory environment. H. pylori infection also weakens mucosal defense by affecting gastric mucosal blood flow and reducing mucus secretion. Because H. pylori is closely linked to ulcer recurrence in children, the high infection rate observed here suggests the need to strengthen eradication therapy and follow-up management. The 63.0 percent infection rate in this cohort is comparable to some previous pediatric studies, though regional prevalence, referral patterns, and diagnostic methods can produce variation — one multicenter study in southern Vietnam reported H. pylori positivity in 93.8 percent of children with peptic ulcers.

Lifestyle habits emerged as significant contributors. The proportion of children attending boarding school was 77.2 percent in the ulcer group versus 28.3 percent in controls, and multivariate regression confirmed boarding status as an independent risk factor with an odds ratio of 2.41. The researchers suggest that collective living environments may involve dietary hygiene issues, irregular daily routines, and psychological stress. Boarding children often face a monotonous diet structure and irregular meal times, which may disrupt the rhythm of gastric acid secretion, while differences in hygiene conditions in collective life may increase the risk of H. pylori infection. High-sugar diets, present in 56.5 percent of the ulcer group versus 28.3 percent of controls, participate in ulcer formation by stimulating gastric acid secretion, affecting intestinal flora balance, and promoting inflammatory responses, with an odds ratio of 2.89. Adjusting diet structure may therefore be an effective prevention strategy. Notably, exercise habits and sleep duration showed no significant differences between the two groups.

Family history of digestive system diseases, reported in 30.4 percent of children with ulcers versus 8.7 percent of healthy children, carried an odds ratio of 3.17, indicating that genetic susceptibility plays an important role. Existing research suggests that certain gene polymorphisms — including cytokine genes such as IL-1β and TNF-α — are associated with H. pylori susceptibility, mucosal repair capacity, and the intensity of inflammatory responses, providing molecular biological evidence for the mechanism of genetic factors. This finding aligns with the broader understanding that pediatric peptic ulcer reflects multidimensional interactions among genetic susceptibility, environmental factors, lifestyle habits, and psychosocial influences, rather than any single cause.

Psychological disorders proved to be the strongest independent risk factor, with an odds ratio of 6.11. Prevalence was 63.0 percent in the ulcer group versus 9.8 percent in controls, and the mean SCARED score — from the Screen for Child Anxiety Related Emotional Disorders, with a threshold of 25 or above indicating psychological disorder — was 28.6 ± 8.4 in the ulcer group versus 14.2 ± 6.1 in controls. The researchers invoke the brain-gut axis to explain this connection: psychological disorders such as anxiety and depression activate the hypothalamic-pituitary-adrenal axis and the autonomic nervous system, increasing vagal nerve excitability, gastric acid secretion, and abnormal gastrointestinal motility. Psychological stress can also affect immune regulation, promote inflammatory responses, and alter intestinal flora composition. Importantly, the brain-gut axis operates bidirectionally — chronic pain and reduced quality of life caused by ulcers may further aggravate psychological disorders, forming a vicious cycle that clinicians should address through psychological health assessment and, where necessary, psychological interventions.

The study has limitations that temper interpretation. As a single-center retrospective case-control analysis, it may be subject to selection and information bias; the healthy controls were recruited from children undergoing physical examination at the same hospital rather than from a community-based population, so hospital population bias cannot be completely excluded. Psychological assessment relied on scale scores rather than clinical diagnostic interviews, which may introduce measurement error, and potential confounders such as environmental factors — air pollution, water quality — were not included. Because of the retrospective design, the observed associations should not be interpreted as causal. Nevertheless, the findings provide evidence-based support for early identification and intervention of pediatric peptic ulcer, suggesting that clinical practice should strengthen screening for high-risk children — those with H. pylori infection, high-sugar diets, boarding status, and psychological disorders — and implement comprehensive interventions including eradication therapy, dietary adjustment, and psychological support to improve prognosis. Future multi-center prospective studies with more comprehensive influencing factors and more precise measurement tools are needed to validate the universality and reliability of these conclusions.

Subject of Research: Clinical features and risk factors for pediatric peptic ulcer in children compared with healthy controls

Article Title: Analysis of clinical feature differences and influencing factors between children with peptic ulcer and healthy children

Article References: Chen, C., & Qiu, H. (2026). Analysis of clinical feature differences and influencing factors between children with peptic ulcer and healthy children. Frontiers in Pediatrics, 14, Article 1849123. https://doi.org/10.3389/fped.2026.1849123

Image Credits: AI Generated

DOI: 10.3389/fped.2026.1849123

Keywords: pediatric peptic ulcer, Helicobacter pylori, duodenal bulb, high-sugar diet, boarding school, psychological disorders, brain-gut axis, SCARED, anemia, retrospective study, logistic regression, gastroscopy