Abstract

F o R over 100 years the treatment of iron deficiency anemia has classically consisted of the oral administration of ferrous sulfate. Therapeutically, results with this inorganic salt have been excellent once the underlying cause of the anemia has been uncovered and eradicated. From the inception of this treatment, however, it has been recognized that the incidence of gastrointestinal side effects has been relatively high. The sequelae may range from the epigastric discomfort, nausea, vomiting, constipation, and diarrhea of therapeutic doses to death in children who have taken toxic amounts of the drug. Deaths of children have been studied by Luongol and found to be caused by a hemorrhagic periportal necrosis. He states that the susceptibility of these areas of the liver is probably due to the proximity of hepatic cells to the portal vein branches which carry the absorbed ferrous sulfate to the liver. He notes further that in sublethal dosage ferrous sulfate toxicity may cause a portal cirrhosis when healing of the damaged liver cells occurs. He also believes that previously diseased liver cells are most susceptible to the toxic action of ferrous sulfate. Recently Berenbaum and co-worker? have performed studies of ferrous fumarate on animals and human beings. Ferrous fumarate is a new organic iron complex which contains a higher iron content than any of the

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