In view of the fact that there exists diverse opinions whether the aplastic and hyperpla.stic types of aplastic anemia are two separate disorders with a similiar clinical picture, or whether these represent a different phase of a single disease, the author carried out a ferrokinetics study by means of the Pollycove method on 29 cases of aplastic anemia with various marrow cellularity in order to see any difference between the aplastic and hyperplastic tyof aplastic anemia on pathophysiology of anemia.
Method of the study is as follows. A complete history and physical examination were carried out on each patient. A diagnosis of aplastic anemia was confirmed based on complete peripheral blood counts and careful bone marrow studies. After a definite diagnosis was established, ferrokinetic studies were performed. Ten to 30 microcuries of radioiron(^(59)Fe) was injected intravenously. During the 10 days folinjection, serial blood samples were analysed for plasma and erythrocyte radioactivity, and in vivo surface measurements of radioactivity over spleen, liver, and sacral bone marrow performed. Hematocrits weredetermined on all samples. Plasma and erythrocyte radioactivity were measured by counting two or three milliliter aliquots in a scintillation well crystal. In vivo skin surface countins were performed by placing scintillation crystal counter with wide angle collimation over liver and spleen in the midaxillary line and in the posterior midline over the upper portion of the sacrum.
According to the formulas, the following ferroindices were derived.
1) Plasma ^(59)Fe disappearance half time
2) Daily hemoglobin synthesis
3) Mean erythron life span
4) Mean effective erythron hemoglobinization time
5) Storage iron exchange rate
6) Net incorporation rate of ^(59)Fe in RBC
The results obtained are as below.
1) Among 29 cases, 12 erythroid aplasia, 7 hypo6 normoplasia, and 4 hyperplasia.
2) Hemoglobin level of hypoplastic group(incluaplasia and hvpoplasia) was 5. 3±2. 3 gm% while that. of hyperplasti.i group (included normoplasia and hyperplasia) was 7.4+2.2 gm%.
3) Serum iron concentration of the hypoplastic group exhibited somewhat higher than those of the hyperplastic group, the former being 216±47 μ%, the latter 190±34 μg%.
4} Plasma ^(59)Fe disappearance half time was markedly prolonged to 287±113 minutes in the hypoplastic group in contrast with that of 122±65 minutes in the hyperplastic group.
5) Net incorporation of 59Fe in RBC of the hypoplastic group was 22±7%, that of the hyperplastic group 27±8%, indicating no significant difference between these two groups.
6) Hemoglobin synthesis in the hypoplastic group was markedly reduced to 0.5±0.2gm per L.per day as compared with 1.4±0.4 gm per L. per day in normal subjects but markedly increased to 6.0+3.1 gm per L. per day in the hyperplastic group.
7) Measurements of daily iron storage deposition showed 14.3±4.6mg in the hypoplastic group and 3.7±4.9 mg in the hyperplastic group.
8) Mean effective hemoglobinization time was normal(1.4±0.2 day) in the hypoplastic group whereas it was markedly prolonged to 3.3±1.1 days in the hyperplastic group.
9) Mean erythron life span was moderately shortened to 61±14 days in the hypoplastic group and markedly reduced to 19±12 days in the hyperplastic group.
10) Plasma radioiron curve revealed slow decrease .of radioactivity with three exponential components in the hypoplastic group but early equilibrium at a relatively high level with two exponential components in the hyperplastc group.
11) In vivo surface measurements showed decreased marrow uptake, progressive accumulation of radioiron in liver and, to a much lesser degree, in spleen in the hypoplastic groups. In the hyperplastic group, the marrow surface radioactivity increased rapidly but was followed by slow and incomplete release from marrow and three different patterns of hepatic and splenic uptakes namely, normal, progressive accumulation and splenic sequestration were noted.
12) It may be concluded that anemia in the hypoplastic group may result frorn an indequate erythropoiesis due to marrow destruction while in the hyperplastic type defective erythropoiesis may be a result of intramedullary hemolysis (ineffective erythropoiesis)
Acknowledgment
The author wishes express his appreciation to Dr. J.E. Varela and Mr. C.R. O´Neal of the Inter-national Atomic Energy Agency for their assistance in this work.
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