Localisation of Uratic Deposits
Uratic deposits evince a decided predilection for cartilages, tendons, muscles, and skin. This localised distribution of the depositions would seem to suggest their dependence on local tissue peculiarities. Now the presence of sodium salts in a solution diminishes the solubility of urates therein. Consequently, in seeking to explain the incidence of tophi, it was suggested that cartilage and tendons, being richer in sodium ions than the blood, this might account for the fact that urates tend to be precipitated in these particular structures.
Again, Almagia, working in Hofmeister’s laboratory, noted that thin sections of cartilage, if left for some hours in a solution of sodium urate, will take up uric acid. Direct inspection readily reveals the presence of white foci and diffuse opacities due to uratic deposits. The marked affinity of normal cartilage for uric acid is again attested by the fact that, given injection thereof in quantity into the peritoneal cavity of rabbits, the uric acid may often be detected by the murexide reaction in joint cartilage, though apparently not in other tissues.
This behaviour would appear to justify the conclusion that the observed accumulation of uric acid in the cartilages in the presence of states of uricæmia, may be explicable on this same basis. In any case, this marked affinity of even normal cartilage for uric acid seems to disprove the necessity of Ebstein’s postulate, viz., that the dissolved uric acid sets up inflammation, and that an antecedent necrosis precedes the deposition of urates. Still, even if we concede the fact that normal cartilage has a marked affinity for uric acid, how is it that in leukæmics, despite their high blood content of uric acid, no uratic deposits ensue? Does not such disparity seem to indicate that in gout some other factor intrudes? in other words, that the excess of sodium ions in particular tissues, while it may favour deposition therein, is inadequate of itself to actually determine the formation of tophi.