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Hypersegmentation in Iron Deficiency Anemia

A. DOSCHERHOLMEN, MD, PhD; K. Mahmud, MD; D. Ripley
JAMA. 1974;229(13):1721-1722. doi:10.1001/jama.1974.03230510013005.
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To the Editor.—  Hypersegmented neutrophils, a hallmark of vitamin B12 and folic acid deficiency, have also been found, for unknown reasons, in chronic renal disease and as a hereditary disorder. The neutrophil hypersegmentation observed in iron deficiency,1 usually ascribed to an associated vitamin B12 or folate deficiency, may also occur without laboratory evidence of deficiency of these vitamins. The reason for this morphologic change in iron deficiency is not known, but abnormalities in folate metabolism have been suggested. Thus, the urinary excretion of formiminoglutamic acid (FIGLU) is often increased in iron deficiency, and experimentally induced iron deficiency may lead to a secondary folate deficiency.2,3In patients with normal serum folate levels, it is possible that a subclinical folate deficiency exists, since iron therapy may induce a fall in serum folate concentrations. It has also been suggested that the enzyme FIGLU transferase is iron-dependent and, therefore, not functioning


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