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Iron deficiency, Helicobacter infection and gastritis.
Acta Haematol. 2009; 122(2-3):97-102.AH

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.

Authors+Show Affiliations

Department of Hematology, Shaare Zedek Medical Center, Jerusalem, Israel. hershko@szmc.org.ilNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

19907146

Citation

Hershko, Chaim, and Aharon Ronson. "Iron Deficiency, Helicobacter Infection and Gastritis." Acta Haematologica, vol. 122, no. 2-3, 2009, pp. 97-102.
Hershko C, Ronson A. Iron deficiency, Helicobacter infection and gastritis. Acta Haematol. 2009;122(2-3):97-102.
Hershko, C., & Ronson, A. (2009). Iron deficiency, Helicobacter infection and gastritis. Acta Haematologica, 122(2-3), 97-102. https://doi.org/10.1159/000243793
Hershko C, Ronson A. Iron Deficiency, Helicobacter Infection and Gastritis. Acta Haematol. 2009;122(2-3):97-102. PubMed PMID: 19907146.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Iron deficiency, Helicobacter infection and gastritis. AU - Hershko,Chaim, AU - Ronson,Aharon, Y1 - 2009/11/10/ PY - 2009/11/13/entrez PY - 2009/11/13/pubmed PY - 2009/12/16/medline SP - 97 EP - 102 JF - Acta haematologica JO - Acta Haematol VL - 122 IS - 2-3 N2 - 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. SN - 1421-9662 UR - https://www.unboundmedicine.com/medline/citation/19907146/Iron_deficiency_Helicobacter_infection_and_gastritis_ L2 - https://www.karger.com?DOI=10.1159/000243793 DB - PRIME DP - Unbound Medicine ER -