Intestinal iron absorption under the influence of available storage iron and erythroblastic hyperplasia

Abstract

A high negative correlation (coefficient ∼ 0.9) between increased ⁵⁹Fe absorption from a diagnostic 0.56 mg ⁵⁹Fe²⁺ dose and the depletion of available storage iron was observed in menstruating and pregnant women, fullterm and premature infants, blood donors, patients with infections, inflammations, tumors, hepatic cirrhosis, gastric surgery, increased urogenital or gastrointestinal blood loss. The increased diagnostic ⁵⁹Fe²⁺ absorption is a reliable and sensitive indicator of at least depleted iron stores or prelatent iron deficiency as caused by iron malnutrition or maldigestion, increased iron requirement in pregnancy, infancy, urogenital or gastrointestinal blood loss. Although the messenger system which signalyzes the depletion of iron stores to the iron absorbing enterocytes of the duodenal and jejunal mucosa is not yet known available storage iron seems to control intestinal iron absorption under normal and the great majority of pathological conditions in humans.

Anemia per se or high erythropoietin levels in blood do not influence iron absorption since patients with even severe erythroblastic hypoplasia, aplastic anemia and megaloblastic anemia due to vitamin B₁₂ deficiency absorb iron according to their iron stores. An only mild hyperplasia of the erythropoietic system in the bone marrow does also not effect iron absorption which was still under the control of available storage iron in patients with hereditary spherocytosis, nonspherocytic congenital hemolytic anemia due to glucose-6-phosphate dehydrogenase deficiency, acquired hemolytic anemia and vitamin B₁₂ deficiency induced megaloblastic anemia.

An exception from the general rule that depleted iron stores do cause increased iron absorption, which can be used therefore for the reliable diagnosis of depleted iron stores or prelatent iron deficiency, was observed only in anemic children with hereditary nonspherocytic enzymopenic hemolytic anemia due to pyruvate kinase deficiency. In these cases a strong normoblastic hyperplasia correlated well with the increased iron absorption in the presence of normal amounts of available storage iron. Blood transfusions which suppress the normoblastic hyperplasia do also reduce the increased iron absorption to normal levels. A similar iron absorption increasing effect of hyperplastic ineffective erythrocytopoiesis was also observed in adults with sideroblastic anemia and children with severe homozygous β-thalassemia although the iron stores of these patients were normal or increased. The messenger system which is used by the body for signalyzing severe normoblastic hyperplasia to the iron absorbing intestinal mucosa and induces a useless and even dangerous augmented iron absorption is not yet known.

Since the diseases with severe normoblastic hyperplasia are extremely rare and easily to diagnose the increased intestinal iron absorption from the diagnostic 0.56 mg ⁵⁹Fe²⁺ dose is a very useful, reliable and sensitive indicator of already the earliest stage of iron deficiency.