638 URIC-ACID METABOLISM AND GOUT 



an absorbable form occurs simultaneously with the attack. The fail- 

 ure of recent studies on the enzymatic transformation of purines to 

 locate anywhere in the human body an enzyme destroying uric acid, 

 makes hazardous the attempt to explain gouty metabohsm as a result of 

 enzymatic abnormalities. However, there can be little doubt that the 

 fundamental reason for the existence of uric acid gout in man lies in the 

 inabilityof the human organism to destroy uric acid. Because man can- 

 not destroy uric acid rapidly by oxidation, as can all other mammals, he 

 is always a potential victim of uric acid retention and deposition. 



It should be mentioned in addition that it is not the uric-acid 

 metabohsm alone that is altered in gout. Irregular periods of nitro- 

 gen retention and nitrogen loss are quite constant features. The 

 cause of this variability, and the form in which the nitrogen is re- 

 tained, are quite unknown, although there is some evidence that the 

 retained nitrogen is in the form of purine bodies (Vogt). ]\Iost of 

 the excessive loss occurs during the acute attacks,"*- and the retention 

 of nitrogen between attacks may be partly to repair the loss; against 

 this, however, is the fact that there is not sufficient gain in weight 

 to account for all of the nitrogen retention. Associated with the de- 

 layed excretion of ingested purines is also a delayed excretion of the 

 other nitrogenous products of protein food.^^ The proportion of 

 purine bases to uric acid, is not altered in gouty urine. ^^^ The state- 

 ments in regard to phosphoric acid elimination, which depends largely 

 on decomposition of nucleins, are contradictory, but it seems probable 

 that it shows no characteristic alterations in gout. Amino acids, espe- 

 cially glycine, are said to be excreted in excess. "^^ There is no significant 

 change in the basal metabolism.'*^ 



It may be seen from the foregoing discussion that we neither under- 

 stand fully the intricacies of metabolism in gout, nor know whether 

 uric acid is responsible for either the acute painful attacks or for 

 the anatomical alterations in the kidneys, heart, and blood vessels. 

 Indeed, Daniels, and McCrudden'*^ have shown that it is possible for 

 gouty patients to have a persistently low content of uric acid in the 

 blood, below the average normal quantity, and to have typical acute' 

 attacks without change in either the uric acid content of the blood or 

 its excretion; attacks were even observed to occur Avhen the blood uric 

 acid was at a subnormal figure from administration of atophan, which 

 increases its elimination. Furthermore, Bass and Horz]')erg"'** found 

 that uric acid can be injected into the blood of gouty subjects until the 

 blood contains as much as 10 mg. per 100 c.c. without causing any 

 joint symptoms. 



« BruKsch, Zeit. exp. Path. a. Tlior., 1906 (2), 610. 



"Leveneand Kristeller, Jour. Exj). Mod., 1912 (16), 303. 



"Hefftor, Dent. Arch. klin. Med., 1913 (109), 322. 



" Bih-ffor and Schwerinor, Arch. exp. Patli., 1913 (74), 353. 



•'« Wentworlli and McClure, Arcli. Int. Med., 1918 (21), 84. 



" Arch. Int. Med., 1915 (15), 1046. 



" Deut. Arch. klin. Med., 1916 (119), 482. 



