370 



ASCORBIC ACID 



operating to cause anemia. The initial reticulocytosis and the increase in 

 indirect reacting bilirubin out of porportion to the extent of the bleeding 

 into the tissues suggests some mechanism for increased blood destruction 

 or faulty utilization of heme pigments in scurvy. The relatively inactive 

 marrow which becomes hyperactive when ascorbic acid is given suggests 

 that ascorbic acid deficiency suppresses marrow activity in some unknown 



T — I — I — I — I I I — I — I I I — n — n — I — I — I — I — I — I — I — I — I — I — r — i — i — r 



*/ll 12 IJ 14 IS 16 I? 18 19 20 tt 22 23 2a 2S 26 2r 28 29 30 VI 2 3 4 5 6 7 6 9 



DAYS 



10 II i; 6/2 



Fig. 16. Hematologic response to ascorbic acid in a patient with severe scurvy 

 and a megaloblastic bone marrow. The reticulocytosis is of the same type that one 

 would expect in a patient with pernicious anemia treated with folic acid or vitamin 

 Bi2. The ascorbic acid in this patient converted the megaloblastic marrow to a normo- 

 blastic one. 



fashion. The megaloblastic features seen occasionally suggest that ascorbic 

 acid deficiency has interfered with the metabolism of folic acid in a patient 

 whose folic acid reserves are badly strained by a grossly inadequate diet. 

 Such a mechanism has been postulated to explain the occurrence of megalo- 

 blastic anemia of infancy.^^ 



However, in scorbutic monkeys, May and his associates'^ have been 

 unable to find any abnormality in protoporphyrin or coproporphyrin and 

 explain the reticulocytosis and increase in urobilinogen on the basis of 

 petechiae and bleeding into the tissues. The scorbutic anemia in their 

 monkeys is hypochromic and the serum iron levels are low, in spite of high 



" E. C. Proehl and C. D. May, Blood 7, 671 (1952). 



