Hermatologic Changes with ACTH and Cortisone Therapy of Rheumatoid Arthritis
Open Access
- 1 November 1951
- journal article
- research article
- Published by American Society of Hematology in Blood
- Vol. 6 (11), 1034-1050
- https://doi.org/10.1182/blood.v6.11.1034.1034
Abstract
1. Detailed hematologic observations, bone marrow aspirations and blood volume determinations were made on 20 patients with rheumatoid arthritis and allied disorders before, during and after the administration of either ACTH or cortisone. 2. Significant reticulocytosis occurred in every patient during therapy, but its magnitude was poorly correlated with either the initial degree of anemia or subsequent increase in circulating red cell mass. 3. There was an increase in hematocrit and total circulating red cell mass of all anemic patients who responded clinically to either ACTH or cortisone. There was little or no improvement of anemia when the clinical response was poor. 4. Polycythemia did not occur in any patient during prolonged therapy or with repeated courses of either ACTH or cortisone. 5. Hemodilution and hemoconcentration were much more profound during and after ACTH administration than they were with cortisone. 6. Bone marrow studies revealed moderate depression of the erythroid series before treatment. At the end of therapy erythroid elements were normal. 7. Significant polymorphonuclear leukocytosis occurred its all patients during therapy while lymphopenia was inconstant and unsustained. Circulating eosinophils were depressed more with ACTH than with cortisone treatment. 8. Before treatment eosinophils and their precursors were present in the bone marrow its normal or increased numbers. During therapy the number of these cells was unchanged in the marrow, even when there was profound peripheral eosinopenia 9. The role of ACTH and cortisone in the physiologic mechanism of hematopoiesis is discussed. 10. The improvement in the anemia associated with inflammatory disease in response to ACTH or cortisone therapy probably is a reflection of the control of the underlying disease rather than a primary "stimulation" of the bone marrow.This publication has 13 references indexed in Scilit:
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