GOUT 513 



nucleins, are contradictory, but it seems probable that it shows 

 no characteristic alterations in gout. 



It may be seen from the foregoing discussion that we neither 

 understand fully the intricacies of metabolism in gout, nor know 

 whether uric acid is responsible for either the acute painful 

 attacks or for the anatomical alterations in the kidneys, heart, 

 and bloodvessels. It is very possible that some entirely different 

 product of metabolism than uric acid is responsible for most of 

 the changes and symptoms of gout 1 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. That 

 it is due to an excess of uric acid in the blood seems to have 

 been excluded, and there is no good evidence that the precipita- 

 tion depends upon a decreased alkalinity of the blood two 

 ideas once in vogue. The local nature of the deposition indi- 

 cates that it must depend upon local changes ; but the hypoth- 

 esis that there occur first degenerative changes in the tissues 

 which determine the precipitation of the urate, seems to have 

 been disproved by the demonstration that the deposition df the 

 urates precedes the necrosis. The histology of urate deposits, 

 both experimental and gouty, has been carefully studied by 

 Freudweiler, 2 His, 3 Kratise, 4 and Rosenbach. 5 



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 deposi- 

 tion, and generally considered as necrotic tissue, merely repre- 

 sents 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 deposition of urates 

 seems to cause such marked symptoms, is also an unanswered 

 question ; unless we accept the explanation that the slower 



1 In swine a " guanin gout " occurs ; see Schittenhelm and Bendix, Zeit. 

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



2 Deut. Arch. klin. Med., 1899 ( 63), 266. 



3 Ibid., 1900 (67), 81. 



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



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



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