Abstract

To the Editor: In 1993, Dufour et al. (1) presented a case of Helicobacter pylori-associated chronic antral gastritis without evidence of bleeding lesions or clinical symptoms other than sideropenic anemia, which was refractory to oral iron administration and subsided only after H. pylori eradication. The authors suggested the possibility of H. pylori gastritis as a sequestering focus for circulating transferrin iron resulting in a vicious cycle, in which iron administration would not replenish iron stores but would enhance H. pylori growth. We have recently detected a case with similar characteristics. An 11-year-old girl was admitted to the hospital because of recurrent abdominal pain. The patient appeared pale on physical examination, which otherwise was unremarkable. Measurement of breath hydrogen revealed lactase deficiency. Abdominal symptoms promptly disappeared after a lactose-free diet was imposed. Results of hematologic studies showed severe hypochromic microcytic anemia (hemoglobin 7.9 g/dl, hematocrit 0.27, mean corpuscular volume (MCV) 71 femtoliters (fl), mean corpuscular hemoglobin (MCH) 21 pg, and 5.6% reticulocytes) caused by iron deficiency (serum iron 14 μg/dl, serum ferritin 10.6 μg/l, serum transferrin 4.02 g/l, 3.5% transferrin saturation). The following tests gave normal or negative results: white blood cell count and differential; platelet count; serum folate; antigliadin and antiendomysial immunoglobulin A antibodies; serum immunoglobulins, transaminases, and urea nitrogen; stool examination for parasites; stool culture; urinalysis; plain abdominal film; abdominal ultrasonography; 99mTechnetium pertechnetate imaging scan for Meckel's diverticulum; and multiple stool examinations for occult blood. Common causes of iron-deficiency anemia (dietary iron deficiency, celiac disease, or other forms of malabsorption, infections, worm or protozoal infestations, tumors, Meckel's diverticulum, blood loss, renal insufficiency) were excluded. Oral ferrous sulfate (4 mg/kg/day) was administered for the next months, but despite continuous and accurate compliance, the serum concentrations of hemoglobin and iron markers were repeatedly and persistently low. Low serum concentrations of hemoglobin (10.9 g/dl), iron (26 μg/dl), and ferritin (4.9 μg/l) persisted after nearly 2 years of iron supply. Levels of serum immunoglobulin G antibody to H. pylori were positive. Findings in upper gastrointestinal fiber endoscopy and biopsy confirmed active chronic antral gastritis and the presence of a large number of H. pylori organisms. Results of the urease test were positive. After treatment with amoxicillin, clarithromycin, and omeprazole, H. pylori was no longer detectable in histologic studies, and urease test results were negative. A few weeks after treatment of H. pylori infection, iron-deficiency anemia began to improve (hemoglobin 11.3 g/dl, serum iron 77 μg/dl, serum ferritin 17.8 μg/l, serum transferrin 2.75 g/l, 28% transferrin saturation). The response to treatment and eradication of H. pylori infection persisted for 1 year after withdrawal of iron therapy. In summary, some patients with H. pylori infection may complain of severe iron-deficiency anemia without evidence of gastrointestinal bleeding. In these cases, treatment of anemia without previous eradication of H. pylori would be ineffective and might contribute to maintaining bacterial growth. Although Dufour et al. (1) have proposed a suggestive explanation for the relationship between H. pylori growth and iron acquisition through a transferrin-mediated mechanism, this etiopathogenic interpretation is hampered by the fact that sideropenic refractory anemia has only been documented in a small number of patients with H. pylori infection. In other cases of H. pylori infection and anemia reported in the literature (2), the etiopathogenic mechanisms leading to anemia are probably related to the presence of bleeding lesions. Jesus Carnicer; R. Badía; J. Argemí Department of Pediatrics Consorci Hospitalari Parc Taulí Sabadell, Spain

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