352 



ASCORBIC ACID 



the affected persons. However, therapeutic trials with ascorbic acid have 

 been disappointing, and, furthermore, low plasma levels are not a satis- 

 factory index of tissue depletion, since tissue levels of mg. % are usually 

 reached before clinical scur\^ occurs. In experimental ascorbic acid de- 

 pletion, gum lesions did not occur,'' occurred rarely,'"* or in more prolonged 

 studies occurred only after the tissue stores of ascorbic acid were exhausted 

 and other scorbutic lesions had been present for many weeks.' ^ In many 

 clinical examples of the disease studied by the author, gum lesions occurred 



ADMISSION OF SCURVY BY MONTHS 

 Cincinnati General Hospital 1935-1950 



II- 

 10 

 9- 

 8 



«. 7 



5 6' 



o 



6 4 

 ^3 



2 



I 







—•Adults 

 --X Infants 



2 < 5 



Month 

 Fig. 5 



only after many other symptoms and signs had appeared. It is doubtful 

 whether chronic gingi\dtis is often related to \atamin C deficiency. 



The first symptoms reported in experimentally mduced scurv}^''- '■* and 

 by patients A\ith the disease are weakness, easy fatigue, and listlessness. 

 These are followed quicklj'- bj'' shortness of breath and acliing in bones, 

 joints, and muscles of the extremities. This aching is worse at night. Appe- 

 tite is moderately reduced, but most patients contiiuie to eat well until 

 swollen painful gums pre^'ent mastication. Tlie skin usuall}'^ becomes dry 

 and rough, dingy, and brown from increasing pigmentation. In a human 

 subject on a diet free of ascorbic acid but adequate m other nutrilites, 



" J. H. Crandon, C. C. Lund, and D. B. Dill, New Engl. J. Med. 223, 353 (1940). 

 »«M. Pijoan and E. L. Lozner, Bull. Johns Hopkins Hosp. 76, 303 (1944). 

 " H. A. Krebs, R. A. Peters, K. H. Coward, L. W. Mapson, L. G. Parsons, B. S. 

 Piatt, J. C. Spence, and J. K. P. O'Brien, Lancet I, 853 (1948). 



