URATE DEPOSITS 639 



It is very possible that some entirely different product of metabo- 

 lism than uric acid is ros|)onsil)lo for most of the chanpos and symi)- 

 toms of gout"'^ — -indeed, this would seem to be the case were it not for 

 the great frequency of the deposition of monosodium urate in the 

 joints and cartilages, both during the acute attacks and in chronic 

 gout. This indicates that there is surely something abnormal in the 

 conditions of uric-acid solution and circulation. Why the urate is 

 precipitated in these definite places is another of the many unsolved 

 problems of gout. The local nature of the depo.sition indicates that it 

 must depend upon local changes; but the hypothesis that there occur 

 first degenerative changes in the tissues which determine the precipi- 

 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 cartilage 

 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 msLy have a higher concentration of uric acid 

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

 out gouty deposits or joint symptoms. Bass and Herzberg'''* 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 

 onl}^ 10 and 8.2 mg. in the blood. Thej^ also found that intravenous 

 uric acid injection caused less uricsemia in the goutj^ 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 care- 

 fuUj' studied by Freudweiler,*" His,»' Krause,"^ and Rosenbach.*^ Their results 

 all indicate that uric acid and urates excite some slight inflamniator\' reaction, 

 cause a slight local necrosis, and seem to act as a weak tissue poison (His). How- 

 ever, they may be deposited without causing necrosis (Rosenbach). Possibly 

 part ot the material observed in areas of urate deposition, and generally considered 

 as necrotic tissue, merely represents the framework of the crystalline 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 de- 

 position of urates seems to cause such marked symptoms, is also an unanswered 

 question, unless 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. *^ 

 Magnus-Levy holds with Pfeiffer, that the local inflammatory 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 fornia- 



*^ In swine a "guanine gout" occurs; see Schittenhelm and Bendix, Zeit. 

 phvsiol. Chem., 1906 (48), 140. 



"=0 Deut. Arch. klin. ISIed., 1899 (63), 266. 



^^ Ibid., 1900 (67), 81. 



" Zeit. klin. Med., 1903 (50), 136. 



5-^ Virchow's Arch., 1905 (179), 359. 



^* Almagia (Hofmeister's Beitr., 1905 (7), 466) has found that joint cartilage 

 placed in urate solutions becomes filled with cr^-stals. which infiltration does not 

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



