IX. EFFECTS OF DEFICIENCY IN HUMAN BEINGS 375 



body and is therefore essential to many different chemical reactions and 

 enzyme systems. It seems probable that this last hypothesis will eventually 

 prove to be correct, but for the present we cannot describe the clinical 

 lesions of ascorbic acid deficiency in terms of al)normalities in specific 

 chemical reactions. 



E. DIFFERENTIAL DIAGNOSIS 



Ascorbic acid deficiency, scurvy, must be differentiated from rickets in 

 infancy. In fact the two diseases commonly occur together and may pro- 

 duce a confusing picture in long-bone x-ray studies. Under these circum- 

 stances the roentgenologic features of rickets overshadow those of scurvy. 

 Rickets interferes with calcification, osteoid is formed normallj^, and the 

 epiphyseal ends of the bones are broadened, mushroomed, and radiolucent 

 as opposed to the white line, the Triimmerfeld zone, and the Geriistmark 

 of scurv}'. The rachitic costochondral junction is swollen and smooth, and 

 the scorbutic one is sharp and indented. The white line of scurvy may 

 resemble superficially the heavy epiphyseal line of lead poisoning. 



Purpura due to thrombocytopenia, either primary, or secondary to in- 

 fectious diseases, the ingestion of drugs, or the replacement of marrow by 

 leukemia or neoplasm may be differentiated from scurvy by the low 

 platelet count, the prolonged bleeding time and clot retraction, and the 

 abnormal serum prothrombin concentration even if the purpura simulates 

 perifollicular hemorrhages. Toxic, embolic, vascular, or allergic purpuras 

 due to drugs, bacterial endocarditis, glomerulonephritis, rheumatic fever, 

 or related diseases such as Henoch-Schoenlein's purpura and disseminated 

 lupus erythematosis, all of which may have superficial similarities to 

 scurvy, may be differentiated from scurvy by finding other signs of the 

 causative disease such as positive blood culture, heart murmurs, high fever, 

 or much blood and other formed elements in the urine. It should always 

 be remembered that scurvy will probably not be manifest if a patient 

 has eaten as much as one or two oranges in the last one or two months. 



The gum lesions of scurvy are mimicked only by dilantin toxicity, and 

 this should be remembered when an epileptic person is found to have 

 scurvy-like gum lesions. Ordinary inflammatory gingivitis is red, scorbutic 

 gingivitis is a bluish-red color, and the gums are much more friable. Gingi- 

 vitis due to ascorbic acid deficiency seldom occurs without other florid 

 manifestations of scurvy.^" 



The muscle pains and swollen joints of some patients with scurvy may 

 suggest rheumatoid arthritis, but patients with arthritis will not usually 

 have bloody joint effusions, or other signs of scurvj', and the scorbutic 

 patient will not have deformities such as are common to rheumatoid 



'» J. S. Restarski and M. Pijoaii, J. Am. Dental Assoc. 31, 1323 (1944). 



