512 URIC-ACID METABOLISM AND GOUT 



a constant diet, and the variations in chronic gout fall within 

 the same limits. There is always an increased amount of uric 

 acid in the blood in gout, but no constant increase can be noted 

 preceding the attack (Magnus-Levy). In the intervals between 

 the 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. 



As yet, however, 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 paroxysm. How- 

 ever, 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 accom- 

 panies 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 retention 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 simultan- 

 eously with the attack. 



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

 metabolism alone that is altered in gout. Irregular periods of 

 nitrogen retention and nitrogen loss are quite constant features. 

 The cause of this variability, and the form in which the nitrogen 

 is retained, are quite unknown, although there is some evidence 

 that the retained nitrogen is in the form of purin bodies (Vogt). 

 Most of the excessive loss occurs during the acute attacks, 1 

 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. The statements in regard to phosphoric 

 acid elimination, which depends largely on decomposition of 



1 Brugsch, Zeit. exp. Path. u. Ther., 1906 (2), 619. 



