282 PYRIDOXINE AND RELATED COMPOUNDS 



The development of pyridoxine deficiency may be accelerated in adults 

 with the use of a pyridoxine analog. Mueller and Vilter described symptoms 

 of pyridoxine deficiency after prolonged administration of desoxypyri- 

 doxine."*' ""'' The pyridoxine analog was given to eight patients suffering 

 from various chronic illnesses in doses of GO to 150 mg. intramuscularly 

 daily for periods of 18 to 55 days, while the subjects were maintained on a 

 diet low in the vitamins of the B complex. 



Seborrhea-like skin lesions developed about the eyes, nose, and mouth 

 within 2 to 3 weeks in seven of the eight patients. In three of the seven the 

 lesions were quite severe. Half of the patients developed erosions in and 

 around the mouth resembling cheilosis of riboflavin deficiency and glossitis 

 resembling morphologically that seen in niacin deficiency. One patient' 

 developed severe systemic symptoms: nausea, vomiting, weakness, and 

 dizziness. The subjects with the most severe manifestations of deficiency 

 were two patients with rheumatoid arthritis. 



There was no anemia due to desoxypyridoxine. The total white count 

 remained unchanged, but in seven of the eight patients there was a mild 

 absolute lymphocytopenia. 



The skin, mucous membrane, and systemic manifestations remained 

 unchanged when a mixture containing thiamine, riboflavin, and nicotina- 

 mide was given, but they disappeared 48 to 72 hours after pyridoxine was 

 administered. 



During the period of the administration of desoxypyridoxine there was 

 no increased excretion of xanthurenic acid in the urine. No tryptophan load 

 test was performed. 



The inhibitory ratio of antimetabolite to metabolite in human beings was 

 not accurately measured but is at least 1:1. 



The pathologic changes and clinical symptomatology observed under 

 the influence of desoxypyridoxine as well as those seen in infants fed for a 

 prolonged period of time a vitamin Be-deficient diet indicate not only the 

 existing need of man for vitamin Be but also give an experimental founda- 

 tion for the clinical and pathologic vitamin Be deficieiuy in man. 



Even before the above-mentioned experimental clinical studies, claims 

 were put forward regarding the usefulness of pyridoxine in various patho- 

 logic conditions in man, with the more or less silent assumption that 

 primary or secondary lack of vitamin Be might play a part in the patho- 

 genesis of these diseases. In other instances pyridoxine was tried thera- 

 peutically in the clinic on the basis of a possibles analogy of the clinical 

 conditions in (juestion to similar manifestations in experimental \ilamin Br, 



"^ J. F. Mueller and R. W. Vilter, J. Clin. Invest. 29, 193 (1950). 

 "^» R. W. ViKer, J. F. Mueller, H. S. Glazer, T. Jarrold, J. Abraham, (\ Thompson, 

 and V. R. Hawkins, /. Lab. Clin. Med. 42, 335 (1953). 



