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Iron Metabolism pp 215–274Cite as

Iron Deficiency

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Abstract

Although it had long been suspected that the cause of iron-responsive anemias was iron deficiency of the organism (Dameshek, 1931; Schulten, 1934), proof was only provided in the 1930s. Chlorosis was ascribed to the disturbed endocrine function of the ovaries (Naegeli, 1931; and others) and the therapeutic effect of iron was believed to be through a stimulatory effect on the pathological bone marrow function that developed as a result of the endocrine disorder. Essential hypochromic anemia was ascribed to “gastrogenic intoxication” (Kaznelson et al., 1929), and it was suggested that the beneficial effect of iron was through the influence of the iron upon the microorganisms of the gastrointestinal tract. M. B. Schmidt (1928) was the first to induce experimental iron deficiency in mice, but he did not believe that humans could suffer from this disorder. In 1936 Heilmeyer and Plötner demonstrated that the level of plasma iron was low in all patients with iron-responsive anemia and was normal or high in those with iron-refractory anemia. They also showed that iron given parenterally disappeared rapidly from the blood in iron-responsive anemias and that iron was poorly absorbed in “gastrogenic” chronic hypochromic anemia or “achlorhydrische Anämie.” They concluded from their findings that the iron-responsive hypochromic anemias were the consequence of iron deficiency. In the next few years the concept of iron-deficiency disease became generally accepted, and the differentiation of the various clinical forms, e.g., chlorosis and idiopathic or essential hypochromic anemia, lost its significance.

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Authors
  1. Iván Bernát M.D., D.Sc.
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© 1983 Akadémiai Kiadó, Budapest

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Bernát, I. (1983). Iron Deficiency. In: Iron Metabolism. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-7308-1_18

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