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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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RED CELLS
Variable hematologic presentation of autoimmune gastritis: age-related progression from iron deficiency to cobalamin depletion
Chaim Hershko,
Aaron Ronson,
Moshe Souroujon,
Itzhak Maschler,
Judith Heyd, and
Julian Patz
From the Department of Hematology, Shaare Zedek Medical Center, Hebrew University Hadassah Medical School, Jerusalem, Israel; Hematology and Gastroenterology Clinics, Meuhedet Health Services, Jerusalem, Israel; and Hematology Clinic and Central Clinical Laboratories, Clalit Health Services, Jerusalem, Israel.
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, patients with IDA were 21 years younger (41 ± 15 years versus 62 ± 15 years) and mostly women. All groups had a high prevalence of thyroid disease (20%) and diabetes (8%) suggestive of the autoimmune polyendocrine syndrome. Stratification by age cohorts from younger than 20 years to older than 60 years showed a regular and progressive increase in mean corpuscular volume (MCV) from 68 ± 9 to 95 ± 16 fl, serum ferritin levels from 4 ± 2 to 37 ± 41 µg/L, gastrin level from 166 ± 118 to 382 ± 299 pM/L (349 ± 247 to 800 ± 627 pg/mL), and a decrease in cobalamin level from 392 ± 179 to 108 ± 65 pg/mL. The prevalence of Helicobacter pylori infection was 87.5% at age younger than 20 years, 47% at age 20 to 40 years, 37.5% at 41 to 60 years, and 12.5% at age older than 60 years. 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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