GOUT 631 



first (lt'<i-('iicrati\(' chaiigcs in the tissues wliit-h deteniiiiKj tlie preeipi- 

 tation of the urate, seems to have been disproved by the demonstra- 

 tion that the deposition of the urates precedes the necrosis. The 

 fact that the presence of other sodium salts in a solution decreases 

 the solubility of urates in that solution, and the fact that cartilaf^e 

 and tendons are richer in sodium salts than the blood, may possibly 

 have something to do with the fact that the urates are precipitated in 

 these particular tissues. On the other hand is the fact that in leu- 

 kemia and nephritis we may have a higher concentration of uric acid 

 in the blood than in gout, and this urictemia may be protracted, with- 

 out gouty deposits or joint symptoms. Bass and Ilerzberg -^'' found 

 that the uric acid content of the joint fluid was approximately the 

 same as that of the blood in patients without gout, although in two 

 gouty uremics they found 18.5 and 20.8 mg. in the joint fluid with 

 only 10 and 8.2 mg. in the blood. They also found that intravenous 

 uric acid injection caused less uric^emia in the gouty, in spite of re- 

 duced renal excretion, and hence they conclude that in gout the tissues 

 have an increased capacity for taking up uric acid. 



The histology of urate deposits, both experimental and gouty, has 

 been carefully studied by Freudweiler,^^ His,-* Krause,-^ and Rosen- 

 bach.^'' Their results all indicate that uric acid and urates excite 

 some slight inflammatory reaction, cause a slight local necrosis, and 

 seem to act as a weak tissue poison (His). However, they may be 

 deposited without causing necrosis (Rosenbach). Possibly part of 

 the material observed in areas of urate deposition, and generally con- 

 sidered as necrotic tissue, merely represents the framework of the crys- 

 talline deposit (Krause). "When experimentally injected, the urates 

 are absorbed slowly by phagocytic leucocytes and giant-cells. Why 

 the gouty tophi can be deposited in the chronic process and cause no 

 pain or inflammation, while in acute gout deposition of urates seems 

 to cause such marked symptoms, is also an unanswered question ; un- 

 less we accept the explanation that the slower rate of deposition and 

 the lack of dissolved urates account for the absence of symptoms with 

 the tophi.-' ]\ragnus-Levy holds with Pfeiff'er, that the local inflam- 

 matory processes must be ascribed to dissolved urates, since they often 

 extend for some distance about the joints, and hence the attack is 

 ascribable to the solution rather than the formation of the deposits, 

 a fact in harmony with the known increased elimination of uric acid 

 during the attack. 



That urates may cause necrosis of the tissues has been definitely 



23 Deut. Aivh. klin. :\red.. ISnO (r..3). 2li(). 



2i Tbid., moo (67), 81. 



25 Zeit. klin. Med., 190.3 (50), 136. 



26VirdH>\v's Arch., lOOo (179). 359. 



2V Almajria (Hofnioistor's Rcitr.. 1905 (7), 466) has found that joint cartilage 

 ]>laee<l in urate solutions becomes fiUed with crystals, which infiltration does not 

 occur with cartilage of anv other origin, or with tendons. 



