GOUT G29 



deficiency in the cliniinatoi-y jjowers (jf the kidneys. There seems to 

 be no particular relation between the amount of uric acid in the blood 

 and the occurrence or severity of attacks.'"'' This uric acid is, ac- 

 cording: to the best evidence, in a free state, and not combined, as was 

 at one time urged by several students of gout. In the intervals be- 

 tween tlie attacks of acute gout the elimination of uric acid remains 

 within the normal limits; however, for a period of one to three days 

 before each acute attack the amount of uric acid is usually decreased 

 considerably. With the onset of the attack the amount of uric acid 

 excreted becomes increased, and for a few days remains above the 

 average, then subsides to about the normal. Of these two features, 

 the increased output of uric acid during the attack seems to be more 

 constant than the reduced output preceding it, but cases occur in 

 which the uric acid excretion shows no variation from that of normal 

 persons. In certain cases of rheumatoid arthritis the behavior of the 

 purine metabolism resembles that of gout.^* 



As yet we have no definite information either as to the cause of 

 this behavior of the uric acid during the paroxysms of acute gout, 

 or as to its part in causing the paroxj^sm. However, in view of the 

 fact that monosodium urate is found in the joints during the attacks, 

 it seems most probable that for some as yet unknown reason there 

 occurs a precipitation or anchoring of the urates in the tissues, which 

 is associated with the attacks of pain and swelling. We do not know, 

 however, that it is the deposition of urates that causes the attacks. 

 Indeed, the fact that uric-acid retention precedes the attack, rather 

 than accompanies it. seems to suggest that it is the absorption of the 

 urate rather than its deposition in the joints that is responsible for the 

 local disturbances. It is also possible that during the period of re- 

 tention the uric acid is held in the blood in some form that cannot 

 be eliminated by the kidney, and that its deposition in the joints in 

 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 metabolism 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 inability of the human organism to destroy uric acid. Because 

 man cannot 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 

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



iTa Pratt, Amer. Jour. Med. Sei., 1916 (151), 92; Bass and Herzherg. Deut. 

 Arch. klin. :\red., 1916 (110). 482. 



18 W. J. Mallory. .Tour. Path, and Bact.. 1910 (15), 207; Ljungdahl, Zeit. klin. 

 Med., 1914 (49), 177. 



