Role of autoimmune gastritis, Helicobacter pylori and celiac disease in refractory or unexplained iron deficiency anemia

Hershko, C.; Hoffbrand, A.Victor.; Keret, D.; Souroujon, M.; Maschler, I.; Monselise, Y.; Lahad, A.

Haematologica 90(5): 585-595

2005


ISSN/ISBN: 0390-6078
PMID: 15921373
Document Number: 586655
Background and Objectives. Conventional endoscopic and radiographic methods fail to identify a probable source of gastrointestinal blood loss in about one third of males and post-menopausal females and in most women of reproductive age with iron deficiency anemia (IDA). Such patients, as well as subjects refractory to oral iron treatment, are often referred for hematologic evaluation.Design and Methods. We prospectively studied 150 consecutive IDA patients referred to a hematology outpatient clinic, screened for non-bleeding gastrointestinal conditions including celiac disease (antiendomysial antibodies), autoimmune atrophic gastritis (hypergastrinemia with strongly positive antiparietal cell antibodies) and H. pylori infection (IgG antibodies confirmed by urease breath test).Results. The mean age of all subjects was 39 18 years and 119 of the 150 patients were female. We identified 8 new cases of adult celiac disease (5%). Forty IDA patients (27%) had autoimmune atrophic gastritis of whom 22 had low serum vitamin B12 levels. H. pylori infection was the only finding in 29 patients (19%), but was a common co-existing finding in 77 (51%) of the entire group. Refractoriness to oral iron treatment was found in 100% of patients with celiac disease, 71% with autoimmune atrophic gastritis, 68% with H. pylori infection, but only 11% of subjects with no detected underlying abnormality. H. pylori eradication in previously refractory IDA patients in combination with continued oral iron therapy resulted in a significant increase in hemoglobin from 9.4 +/- 1.5 (mean 1SD) before treatment to 13.5 +/- 1.2 g/ dL (p < 0.001 by paired t test) within 3 to 6 months of treatment.Interpretation and Conclusions. The recognition that autoimmune atrophic gastritis and H. pylori infection may have a significant role in the development of unexplained or refractory IDA in a high proportion of patients should have a strong impact on our daily practice of diagnosing and managing IDA.

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