Iron-deficiency anemia associated with Helicobacter pylori gastritis
M Konno1, S Muraoka, M Takahashi
1Department of Pediatrics, Sapporo Kohsei General Hospital, Japan.
Insights
Helicobacter pylori infection is linked to iron-deficiency anemia (IDA) in children. Eradicating H. pylori successfully resolved IDA in all studied cases, suggesting a causal relationship.
Area of Science:
- Pediatric Gastroenterology
- Infectious Diseases
- Hematology
Background:
- Emerging evidence suggests a connection between Helicobacter pylori infection and iron-deficiency anemia (IDA).
- This study reports on six pediatric cases of IDA associated with H. pylori gastritis.
Purpose of the Study:
- To investigate the association between H. pylori infection and IDA in pediatric patients.
- To evaluate the efficacy of H. pylori eradication therapy in resolving IDA.
Main Methods:
- Six patients (5 boys, 1 girl; mean age 13.6 years) with IDA underwent extensive gastrointestinal work-up.
- H. pylori infection was confirmed via biopsy and rapid urease testing.
- Patients received a 2-week course of lansoprazole, clarithromycin, and metronidazole without iron supplementation.
Main Results:
- Endoscopy revealed antral nodularity but no bleeding lesions in all patients.
- H. pylori was successfully eradicated in all six cases.
- No evidence of IDA was found during follow-up examinations ranging from 27 to 50 months post-treatment.
Conclusions:
- H. pylori infection may be a contributing factor in unexplained cases of IDA.
- Successful eradication of H. pylori can lead to the resolution of iron-deficiency anemia.
Background:
Recent studies have suggested an association of Helicobacter pylori and iron-deficiency anemia (IDA). This is a report of six cases of IDA associated with H. pylori gastritis.
Methods:
Six patients with IDA were studied (5 boys and 1 girl; mean age 13.6 years; range 13-15 years). Five had a medical history of long-standing IDA and of oral iron supplementation at outpatient clinics. The anemia recurred after the iron therapy had been discontinued. The sixth patient was admitted to the hospital with severe IDA. An extensive work-up was ordered that included technetium-99m (99mTc) scans for Meckel's diverticulum, total colonoscopy, and gastrointestinal endoscopy. After biopsy-based H. pylori test results were confirmed to be positive, anti-H. pylori therapy consisting of lansoprazole, clarithromycin, and metronidazole was administered for 2 weeks with no iron supplementation. The hematologic profile and iron status were assessed periodically after the end of the eradication regimen.
Results:
Upper gastrointestinal endoscopy revealed a marked antral nodularity but no evidence of bleeding lesions in all the patients. Given the histology and the fact that rapid urease test results were positive, chronic active gastritis with H. pylori was diagnosed in all these cases. H. pylori was successfully eradicated in all the patients. There was no evidence of IDA in any of the follow-up examinations between 27 and 50 months after anti-H. pylori therapy.
Conclusions:
H. pylori infection may be involved in cases of IDA of unknown origin, and the eradication of H. pylori can be associated with the resolution of anemia.
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