Stickney, J.M.

THE RECENT publications of Farber and co-workers dealing with the treatment of acute leukemia in children have awakened widespread interest. Their investigations have stimulated hope for the amelioration of symptoms of this fatal disease and indicated the possibility of provoking remissions that lengthen the lives of those patients affected by it, while making them more comfortable at the same time. In investigating leukemia and allied conditions of a neoplastic nature, Farber and co-workers noted what they termed an "acceleration phenomenon" in the blood and bone marrow of leukemic children treated with folic acid or its conjugates such as diopterin (pteroyldiglutamic acid) or teropterin (pteroyltriglutamic acid). There was marked hyperplasia of the marrow as well as of other sites of leukemic involvement at postmortem examination. They reasoned that if folic acid or its conjugates speeded up the leukemic process, an antagonist to folic acid might be devised in order to retard the progress of the disease or stop it altogether. Through co-operation with the research division of one of the major pharmaceutical firms, a series of folic acid antagonists was soon developed. One of these was aminopterin (4-aminopteroylglutamic acid). It differs from folic acid only in the substitution of the NH2 group for the OH radical in the fourth position of the pteridine group. Of several compounds synthetically made, it has been the most effective and yet most toxic agent in its action on the leukemic process. Farber and co-workers first employed aminopterin in the treatment of acute leukemia of children in December 1947.

Abstract In our experience, in half of the cases of primary hemolytic anemia in which there is no family history of anemia, jaundice or splenomegaly, examination of the blood disclosed microspherocytic erythrocytes and increased fragility of erythrocytes. The results of splenectomy in these cases are better than in those in which microspherocytosis is absent. True macrocytosis was observed in only one instance. Females predominated in both groups of cases. Agglutinins and hemolysins have not appeared to play any significant role in the production of the hemolytic syndrome in our cases. We do not feel justified in expressing an opinion as to whether the microspherocytosis indicates a familial or congenital blood disorder. From a practical standpoint, it makes no great difference since splenectomy should be considered seriously in any case of chronic primary hemolytic anemia. It may be of value in some cases of secondary or symptomatic hemolytic anemia.

Abstract Ulceration of the skin of the legs may occur in Mediterranean disease. Such ulceration cannot be distinguished grossly from that occurring in sickle cell anemia and congenital hemolytic icterus. The outstanding histologic feature (noted at biopsy of one of these ulcers) is the prominent deposition of iron in the cutis.