Paper

Iron Deficiency, Helicobacter Infection and Gastritis
Chaim Hershko^{a, b}, Aharon Ronson<sup>a, c

a</sup>Department of Hematology, Shaare Zedek Medical Center,
^bHematology Clinic and Central Clinical Laboratories, Clalit Health Services, and
^cHematology Clinics, Meuhedet Health Services, Jerusalem, Israel

Address of Corresponding Author

Acta Haematol 2009;122:97-102 (DOI: 10.1159/000243793)

  Key Words

• Autoimmune atrophic gastritis
• Celiac disease
• Gastritis
• Helicobacter
• Iron deficiency anemia
• Vitamin B₁₂

  Abstract

Despite elegant regulatory mechanisms, iron deficiency anemia (IDA) remains one of the most common nutritional deficiencies of mankind. Iron deficiency is the result of an interplay between increased host requirements, limited external supply, and increased blood loss. When related to increased physiologic needs associated with normal development, iron deficiency is designated physiologic or nutritional. By contrast, pathological iron deficiency, with the exception of gross menorrhagia, is most often the result of gastrointestinal disease associated with abnormal blood loss or malabsorption. If gastroenterologic evaluation fails to disclose a likely cause of IDA, or in patients refractory to oral iron treatment, screening for celiac disease (anti-tissue transglutaminase antibodies), autoimmune gastritis (gastrin, anti-parietal or anti-intrinsic factor antibodies), and Helicobacter pylori (IgG antibodies and urease breath test) is recommended. Recent studies indicate that 20–27% of patients with unexplained IDA have autoimmune gastritis, about 50% have evidence of active H. pylori infection, and 4–6% have celiac disease. The implications for abnormal iron absorption of celiac disease or autoimmune gastritis are obvious. In patients with unexplained IDA and H. pylori infection, cure of refractory IDA by H. pylori eradication offers strong evidence for a cause-and-effect relation between H. pylori infection and unexplained IDA. Stratification by age cohorts in autoimmune gastritis implies a disease presenting as IDA many years before the establishment of clinical cobalamin deficiency. It is likely caused by an autoimmune process triggered by antigenic mimicry between H. pylori epitopes and major autoantigens of the gastric mucosa. Recognition of the respective roles of H. pylori and autoimmune gastritis in the pathogenesis of iron deficiency may have a strong impact on the diagnostic workup and management of unexplained, or refractory IDA.

Copyright © 2009 S. Karger AG, Basel

  Author Contacts

C. Hershko
Department Hematology
Shaare Zedek Medical Center, POB 3235
IL–91031 Jerusalem (Israel)
Tel. +972 2 655 5567, Fax +972 2 570 0693, E-Mail hershko@szmc.org.il

  Article Information

Published online: November 10, 2009
Number of Print Pages : 6
Number of Figures : 0, Number of Tables : 1, Number of References : 50