Table II.—Concentration of Uric Acid in Miscellaneous Human Tissues per 100 Grams of Material

Tissue.Uric
acid.
mg.
Pectoral muscle2·5
Uterine muscle2·0
Uterine muscle2·5
Uterine muscle1·2
Mixed tonsils1·7
Thyroid0·0

Again, as before alluded to, Bass and Herzberg found that intravenous injection of uric acid caused less uricæmia in the gouty, despite diminished renal excretion. Hence, they concluded that in gout the retention capacity of the tissues for uric acid is augmented.

Fürth, an ardent advocate of Umber’s hypothesis, emphasises the fact that Wiechowski was never able to detect any evidence of uricolysis in the human body. Continuing, he observes, if we reject all idea of uric acid retention in the tissues, “It would be a particularly difficult thing to understand why gouty patients do not simply expel by a compensatory hyper-excretion the uric acid which is accumulated from a supposed failure of uricolysis; precisely as in leukæmia the patient compensates simply by an exaggerated excretion of the excessive uric acid which is mobilised in the body from the excessive purin decomposition.” His conclusion, therefore, is that, “In the gouty individual there must exist some cause which makes a compensatory uric acid excretion impossible; and that is plainly a retention affinity of the tissues, because of which the uric acid is actually held in the tissues.

In light of Fine’s revelations the retention capacity of the bodily tissue for uric acid may, we take it, be considered as fairly well established. But, in view of the precipitation or anchoring of urates in the tissues in gout it is most desirable that further investigations be made to discover whether in gouty subjects the tissue retention capacity for uric acid is enhanced.

“The impression,” says Fürth, “grows on one that this hitherto little considered factor, of an increased affinity of the tissues for uric acid in the gouty subject is very much closer to the real kernel of the gout problem than, for example, the question of the fixation of uric acid in the blood about which there has been so much contention, and with which of necessity we are compelled, at least, to some little extent to concern ourselves.” The results of modern researches tend to support this more catholic conception. We would recall that Lewis and his co-workers, seeking the source of the increased endogenous purin excretion that follows ingestion of purin-free food, were forced to reject the view that it was solely derived from katabolism of the nuclear substance of the digestive glands, and to refer it instead to “wear and tear” of the body cells as a whole. Precisely the same change in attitude, we may remind our readers, has overtaken us in regard to the site of urea formation, viz., that not only the liver cells, but those of the muscles also participate in its production.

While admitting that dogmatism is out of place, still to our mind this theory of tissue retention makes strong appeal. In light of it the nebulous “gouty diathesis” seems on its way to become incarnate in some inborn peculiarity of tissue-function, a falling short of full physiological activity, or, as M. Rendu termed it, a “primordial vice of nutrition.”

In other words, in gout there is no rift nor lack of finish in the orderly sequence of enzymatic reactions that eventuate in uric acid. Uric acid is formed and, as far as we know, after a normal fashion. But, here comes the flaw, viz., the uric acid, when formed, fails of transport and elimination. It is precipitated and anchored in the tissues, from whose grip it fails to detach itself. In short, it is not the formation of uric acid, or its failure of further metamorphosis, but the retention of uric acid, and more pertinently, its fixation in the tissues that constitutes the salient feature of gout.

Now, all modern research tends to indicate that uric acid is not an intermediary, but a terminal product of metabolism, and, moreover, that there are no uricolytic ferments within the body whereby its destruction can be accomplished.

If we grant that—