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Blood, 15 February 2006, Vol. 107, No. 4, pp. 1673-1679.
Prepublished online as a Blood First Edition Paper on October 20, 2005; DOI 10.1182/blood-2005-09-3534.
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Submitted September 1, 2005
Accepted October 9, 2005
Variable hematological presentation of autoimmune gastritis:age-related progression from iron deficiency to cobalamin depletion
Chaim Hershko*, Aaron Ronson, Moshe Souroujon, Zhao Maschler, Judith Heyd, and Julian Patz
Department of Hematology, Shaare Zedek Medical Center, Jerusalem, Israel; Hematology Clinic and Central Clinical Laboratories, Clalit Health Services, Hebrew University Hadassah Med. School, Jerusalem, Israel
Hematology and Gastroenterology Clinics, Meuhedet Health Services, Jerusalem, Israel
Hematology Clinic and Central Clinical Laboratories, Clalit Health Services, Hebrew University Hadassah Med. School, Jerusalem, Israel
* Corresponding author; email: hershko{at}szmc.org.il.
Iron deficiency is a known complication of achlorhydria and may precede the development of pernicious anemia. Among 160 patients with autoimmune gastritis identified by hypergastrinemia and strongly positive antiparietal antibodies, we explored the overlap between 83 subjects presenting with iron deficiency anemia (IDA), 48 with normocytic indices and 29 with macrocytic anemia. Compared with macrocytic patients, IDA patients were 21 y younger (41±15 vs 62±15 y) and mostly female. All groups had a high prevalence of thyroid disease (20%) and diabetes (8%) suggestive of the autoimmune polyendocrine syndrome. Stratification by age cohorts from < 20 to >60 y showed a regular and progressive increase in MCV from 68±9 to 95±16 fl, serum ferritin from 4±2 to 37±41 µg/L, gastrin from 349±247 to 800±627 u/mL , and a decrease in cobalamin from 392±179 to 108±65 pg/mL. The prevalence of H pylori infection was 87.5% at age < 20 y, 47% at 20-40 y, 37.5 % at 41-60 y and 12.5% at age > 60y. These findings challenge the common notion that pernicious anemia is a disease of the elderly and imply a disease starting many years before the establishment of clinical cobalamin deficiency, by an autoimmune process likely triggered by H pylori.
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