632 URIC-ACID METAIiOl.lsU AM) GOUT 



established, and this may lead to conneetive-tissiie formation and 

 contraction.-* But the actual increase of uric acid in the blood and 

 tissues in gout is so slight that we are not warranted in saying that 

 the usual tendency to sclerosis in all the organs in gout is due to the 

 action of uric acid, rather than to some other unknown agent or agents. 

 Excess of uric acid in the blood is by no means pathognomonic of gout, 

 for we may have relatively great excesses of uric acid in the blood in 

 leukemia, in some cases of nephritis, and after eating large amounts 

 of nucleoproteins, without a symptom of gout. Furthermore, it is 

 quite possible that the precursors of uric acid, the purine bases, are 

 responsible for more harm than the uric acid itself. Thus, admin- 

 istration of adenine to dogs and rabbits will ])roduce degenerative 

 changes in the kidneys, associated with the de])osition of substances 

 resembling uric acid and urates in the renal tissue; and ]\Iandel ^'^ 

 states that purine bases may cause fever, independent of infection. 

 In this connection it may be mentioned that many have looked upon 

 renal alterations, leading to failure of excretion of uric acid, as the 

 primary cause of gout ; but the evidence in favor of this is faulty, be- 

 cause frequently renal changes are slight or entirely absent in *gout, 

 whereas marked nephritis of all forms may exist without the co- 

 existence of gout, and, as mentioned above, the kidney in gout shows 

 no lack of ability to excrete uric acid injected into the tissues. ]\Iag- 

 nus-Levy, however, seems to believe that a renal retention of uric acid 

 is of importance, and that it may occur without morphological changes 

 in the kidneys. 



The newer methods of blood analysis (Folin) have given support 

 to this view. Fine '^^ especially calls attention to the fact that in 

 early interstitial nephritis the blood shows a greater increase in uric 

 acid than in urea or creatinine, as if the diseased kidney found more 

 difficulty in excreting uric acid than the other substances.-^'' As a 

 result the blood in early nephritis may show quite the same figures for 

 uric acid, urea and creatinine as are found characteristically in gout. 

 Although a few observers have occasionally found normal amounts of 

 uric acid in the blood in gout, this seems to be exceptional. Hence 

 we are still confronted with the question whether gout is anything 

 more than a form of nephritis in which uric acid excretion is chiefly 

 impaired, or whether there does exist a special disease, gout, which 

 causes uric-acidemia more or less independently of renal abnormalities. 



2R Ueeause the fjoiitv toplii do not siippurato, even wlicn ulcoratod tliroucrli the 

 skin, it has boon susrsrestod that the urates have antisejitic projierties. 'Bendix 

 (Zeit. klin. IMed., 1902 (44). 16.'i), however, could not donionstrate such antiseptic 

 ])roperties experimentally. Xo* a1'"avs do tlie tophi consist solely or even lar<rely 

 of urate's, hut these inav he replavcd h\- calciniii salts ( Kaliii. Arcli. Iiil. ^led., 

 ini3 (11), 92). 



2!> Arncr. Jour. Phvsiol., 1904 (10), 4r)2 ; 1907 (20), 4:?9. 

 ■' 2fiH .Tour. Anier. :\Ied. Assoc. lOlH ((JO), 20.')1. 

 • 20b See also Denis, Jonr. Hiol. Chein.. 191.5 (2.'?). 147. 



