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Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
A Five-Year-Old Boy with Marked Hypergastrinemia Associated with H. pylori Infection
Asako Nakata1, Hitoshi Tajiri, Yuri Etani
1Department of Pediatrics, Osaka General Medical Center, Osaka, Japan.
Insights
Persistent epigastric discomfort in a child was linked to high gastrin levels caused by Helicobacter pylori infection. Eradication therapy successfully normalized gastrin levels, suggesting H. pylori as a cause of hypergastrinemia.
Area of Science:
- Pediatric Gastroenterology
- Endocrinology
- Infectious Diseases
Background:
- Hypergastrinemia in children can present with non-specific symptoms like epigastric discomfort.
- Differential diagnosis includes gastrinoma and infections like Helicobacter pylori.
- Evaluating pediatric hypergastrinemia requires a comprehensive approach.
Observation:
- A 5-year-old boy presented with persistent epigastric discomfort and significantly elevated serum gastrin levels.
- Diagnostic workup, including calcium injection tests and CT scans, ruled out gastrinoma.
- Helicobacter pylori infection was confirmed via urea breath test and fecal antigen test.
Findings:
- H. pylori eradication therapy led to normalization of gastrin levels and improvement in pepsinogen parameters.
- Immunohistochemical analysis suggested reduced somatostatin secretion due to decreased D cell population contributed to hypergastrinemia.
- These findings indicate H. pylori infection as a potential cause of marked hypergastrinemia in children.
Implications:
- H. pylori infection should be considered in the differential diagnosis of pediatric hypergastrinemia.
- Therapeutic diagnosis via eradication therapy can be a valuable tool.
- Immunohistochemical examination aids in understanding the mechanism of hypergastrinemia in such cases.
Abstract:
A 5-year-old boy was referred to our department for persistent epigastric discomfort. Serum gastrin level was 635 pg/ml with a pepsinogen (PG) I level of 102.7 ng/ml and a PG I/II ratio of 23.2, indicating a hyperacidic state. Upper gastrointestinal endoscopy showed normal gastric mucosal folds and no abnormalities including no gastric mucosal atrophy. To investigate the cause of hypergastrinemia, a Ca injection test was performed and the patient showed no definitive response to a large load of Ca. Contrast-enhanced dynamic CT revealed no space-occupying lesions. The results from these two studies were not consistent with the presence of gastrinoma. A urea breath test showed 2.8%, and a test for the fecal H. pylori antigen was positive. Since H. pylori infection was considered to be a possible cause of hypergastrinemia, eradication therapy was introduced. The therapy was shown to be successful by using a repeated urea breath test that showed a normalization to 0.6%. 7 months after the therapy blood examination showed a gastrin level of 191 pg/ml, a PG I level of 36.7 ng/ml, and a PG I/II ratio of 7.3. An immunostaining study of the gastric mucosa suggested that a decrease in somatostatin secretion due to a reduction in D cell population might have induced hypergastrinemia in this case. In children with H. pylori infection showing marked hypergastrinemia, immunohistochemical examination and therapeutic diagnosis by eradication may be helpful in the differential diagnosis of gastrinoma.
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