IX. EFFECTS OF DEFICIENCY IN HUMAN BEINGS 371 



iron intake, orally or parentorally, a feature which they explain on the 

 basis of poor iron absorption, blood loss, and "stress." This anemia of 

 scurvy in monkeys reproduces the hypochromic anemia seen in scorbutic 

 infants but not the normochromic, normocytic, or slightly macrocytic 

 anemia found in adult persons with scurvy. 



It is probable that the anemia of scurvy depends upon the interaction 

 of ascorbic acid deficiency and multiple dietary inadequacies on bone mar- 

 row function, yet ascorbic acid alone will restore these failing metabolic 

 reactions. Therefore, the author believes that ascorbic acid has a direct 

 effect on blood formation. 



Other indirect effects of ascorbic acid on l)lood formation have been 

 reported from time to time in the literature. Pernicious anemia and related 

 macroc>'tic anemias in persons with severe ascorbic acid depletion or frank 

 scurvy may not respond to refined liver extract until ascorbic acid is given. 

 An interesting report from England describes relapses in three persons with 

 pernicious anemia during the winter of 1941 when the English diet was 

 severely lacking in ascorbic acid. Adpiinistration of this vitamin restored 

 the effectiveness of the liver extract. ^^ 



Reticulocytosis and erythrocyte responses have been occasionally re- 

 ported in persons with pernicious anemia and related macrocytic anemias 

 following treatment with large doses of ascorbic acid.^^ Very low plasma 

 and white lilood cell-platelet ascorbic acid levels have been found in 20 

 unselected patients with pernicious anemia, none of whom had the clinical 

 signs of scurvj'.*® These incidents support the concept of the biochemical 

 interrelationship of ascorbic acid, folic acid, and vitamin B12 to which 

 reference has already been made. 



Ascorbic acid has no beneficial effect in the anemias of infection, rheuma- 

 toid arthritis, iron deficiency, chronic blood loss, or leukemia. 



D. PATHOLOGY AND PATHOLOGIC PHYSIOLOGY 



The fundamental pathologic change in ascorbic acid deficiency occurs 

 in tissues of mesenchymal origin and is best exehiplified in newly formed 

 fibrous tissues. *^"*^ The same type of alteration occurs in teeth, growing 

 bone, and blood vessel walls, and accounts for the changes observed in these 

 structures by the clinician. 



In connective tissue the fibroblast lies in an amorphous ground substance 



" S. C. Dyke, B. L. Delia Vida, and E. Delikat, Lancet II, 278 (1942). 



" R. W. Vilter, Syttiposia on Nutrition I, 179 (1947). 



'* R. O. Wallerstein, J. W. Harris, and G. Gabuzda, Proc. Am. Fed. Clin. Research 



Abstr. 119, (1952). 

 "S. B. Wolbach and O. A. Bessey, Physiol. Revs. 22, 233 (1942). 

 '8S. B. Wolbach, J. Am. Med. Assoc. 108, 7 (1937). 

 *' G. Dalldorf, The Vitamins, p. 339. American Medical Association, 637 pp., 1939. 



