(2) That the relatively high sodium content of certain tissues, e.g., cartilage, favours the incidence of uratic deposits therein.
(3) That tissue necrosis is not necessarily an antecedent to uratic deposits.
(4) That no relationship can be established between the incidence or multiplicity of tophi and uricæmia.
It will be seen from these conclusions that the proximate cause responsible for the genesis of tophi is yet to seek, and in pursuance of our quest we turn to another aspect of this complex subject.
Tissue Affinities for Uric Acid
Injecting uric acid intravenously into gouty subjects, Umber noted that at times the whole was retained, but on some occasions was excreted in fractional portions. On the other hand, a normal individual under similar circumstances eliminates it completely. In explanation thereof, he proffered the opinion that this failure on the part of gouty persons to excrete exogenous uric acid was due to a special affinity of their tissues for uric acid.
As to intravenous injection of uric acid, however, modern investigation has established that, both in normal as well as gouty subjects, its excretion is spread over several days, and the whole is not recoverable from the urine. Now this incomplete excretion or retention of uric acid was attributed to defective elimination by the renal cells; but, as shown in a previous chapter, this conception fails of demonstration. Nor, for that matter is there any proof either that the retention is due to fixation of the uric acid in the blood serum. Accordingly, to our minds, it is permissible then to canvass the further possibility adumbrated by Umber, viz., that an increased affinity of the tissues for uric acid may haply account for the diminished purin excretion, the excess of uric acid in the blood, lymph, and tissues, and that these same may lead to uratic deposition.
This last hypothesis derives colour from the findings of Schmoll, Magnus Levy, Vogt, Reach and Bloch, who noted that, after giving thymus to gouty persons, they found far less uric acid in the urine than in the case of normal subjects. Also, that the ingestion of thymus by the victims of chronic gout repeatedly resulted in acute outbursts of the disease. Moreover, as we saw when discussing the sources of uric acid, there are cogent reasons for avoiding a too restricted conception which would make the leucocytes, the muscles, or the digestive glands alone responsible for the endogenous production of uric acid; in other words, that a more catholic attitude on our part is indicated, one which would envisage it as the outcome of continuous and general cellular wear and tear. That an increased cellular destruction, as induced experimentally, e.g., by exposure to Röntgen rays, is capable of raising the blood content of uric acid in a gouty subject, and of precipitating a gouty paroxysm, may be inferred from the researches of P. Linsen.