Unexplained Refractory Iron-Deficiency Anemia Associated with Helicobacter pylori Gastric Infection in Children: Further Clinical Evidence


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Helicobacter pylori infection in children has mostly been associated with recurrent abdominal pain, gastric dyspepsia, or duodenal ulcer. Uncommon clinical features such as protein-losing enteropathy (1) and malabsorption (2) have also been reported.In 1993 we first described a case of iron-deficiency anemia (IDA) not due to any conventional cause, which was associated with H. pylori gastric infection (3). The anemia was refractory to iron therapy and reversed only after bacteria eradication, thus suggesting possible interference of H. pylori in iron metabolism. In this article we describe four consecutive similar cases observed since then. To understand the possible pathogenic role of H. pylori in the development of the anemia, extensive investigations have been undertaken, and the internal cycle of iron metabolism has been studied in all patients.CASE REPORTSCase 1A 4-year-old boy was admitted to a local hospital for severe IDA (hemoglobin, 5.9 g/dl) without gastrointestinal symptoms. After a packed red cell transfusion, he was discharged with a diagnosis of IDA of unknown origin. One year later (October 1991), he was admitted to our institution because of inefficacy of oral and intramuscular injections of iron. On examination he appeared pale and in poor general health. His weight was 15 kg (-3 standard deviations [SD]), height 102 cm (-3 SD). The hematologic profile showed persistent IDA (Table 1). Findings in an extensive initial work-up (including erythrocyte sedimentation rate; levels of C-reactive protein, total serum proteins and immunoglobulins; D-xylose absorption test; IgA antigliadin and antiendomysial antibody tests; bilirubin, lactate dehydrogenase, folate, B12 vitamin, and hemoglobin electrophoresis; multiple stool examinations for ova, parasites, and occult blood; barium meal and follow-through; technetium-99m pertechnetate imaging scans for ectopic gastric mucosa and occult gastrointestinal blood loss) and iron absorption test (Table 2) were all normal. Oral iron polimaltosate was administered (5 mg/kg daily elemental iron), but after 2 months of therapy, hemoglobin was unchanged, and the patient was readmitted for re-evaluation. IgG antibody titer to H. pylori (enzyme-linked immunosorbent assay; Helori-test, Eurospital, Trieste, Italy; normal value, <15%) was 71%. Findings in upper gastrointestinal endoscopy were normal. A rapid urease test result was positive. Histology showed H. pylori-positive chronic superficial antritis and normal duodenal mucosa. Analysis of bone marrow aspirate indicated a 4:1 myeloid-erythroid ratio with substantially normal morphology. Pearl's staining showed no detectable iron. After an internal iron cycle study (Table 3), a 1-month course of 50 mg/kg amoxicillin daily and 200 mg/m2 colloidal bismuth subcitrate daily was administered without iron supplement. After this therapy, no changes were observed in the patient's hematologic profile and iron stores. The child was then given 500 mg of intramuscular iron polimaltosate over 3 weeks. Three months later, H. pylori was no longer detectable in gastric histology and hematologic and iron profiles were normal (Table 1). They remained so after 3 years, as did the IgG antibody titer to H. pylori.Case 2Iron-deficiency anemia developed in a boy aged 13 years, 7 months (hemoglobin, 9 g/dl) without gastrointestinal symptoms. After 2 months (September 1992), because there was no response to oral therapy with 100 mg/day of ferrous sulfate administered for 1 month, he was referred to our institution. On examination he appeared pale but in good general health; his weight was 48 kg (50th percentile), height 155 cm (25th percentile), Tanner pubertal stage P5.

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