The sum of our reflections is that the _toxicity_ of uric acid has been grossly over-estimated, and that, like its relative _urea_, it is practically _non-irritating_ and _inert_; in other words, it cannot any longer be regarded as the _essential cause_ of the _acute_ or _chronic_ forms of _gout_, whether of _articular_ or _ab-articular_ site. Moreover, far from its presence in excess in the blood being pathognomonic of gout, it must, as Walker Hall contends, be held merely “as symptomatic of conditions which help or prevent its solubility and excretion and does not itself cause lesions which accompany uricacidæmia.” ARE THE PRECURSORS OF URIC ACID TOXIC? Naturally the upholders of the uric acid theory were loth to find their fetish uric acid was allotted a meaningless _rôle_. That it should be deemed inert was to dislodge the very corner-stone of the imposing superstructure they had been at such pains to raise. Uric acid not responsible for the genesis of gout! But, haply, maybe their position was still unassailable; for what of the purin _bases_, the forerunners of uric acid? Might not the blame lie with these? Straightway _xanthin_, _hypoxanthin_, _adenin_, etc., were credited with pernicious potencies.[26] Nor did they lack apparent support from the experimental side. Thus, Mandel affirmed that purin bases, apart from infection, might originate pyrexia. Others, again, noted that in dogs and rabbits fed on adenin, degenerative changes in the _kidneys_ ensued, with deposits resembling uric acid and urates in their substance. The fact, too, that _guanin-gout_ was occasionally met with in swine, also lent colour to their views. Moreover, that ingestion of these congeners of uric acid led in animals to renal lesions, seemed to support the contention of many, that renal disorder might be the primary cause of gout. But, unfortunately, Kolisch and Weintrand’s assertion that the alloxur bases were found in increased quantities in the urine of gouty patients was contradicted by Schmoll, His, Laquer, and others. Still more cogent, apparently, the announcement in 1910, by Brugsch and Mallory, that they had seen a typical attack of gout ensue in a gouty patient in sequence to a dose of 0·5 gram of _hypoxanthin_. Nor did this reaction of gouty persons fail of confirmation, as in the same year, Brugsch and Schittenhelm, in gouty patients, noted attacks of arthritis, after the administration of _nucleinic acid_. Nevertheless, we must beware of laying too much stress on isolated experiments of this nature, so hypersensitive are some of the victims to any strange or unaccustomed ingesta. Were all the myriad other determinants of gouty attacks eliminated, over-drinking, trauma, mental disturbances, etc.? for be it recollected, all the victims of these experiments with _hypoxanthin_ and _nucleinic acid_ were _gouty_ subjects, _i.e._, potentially liable to attacks at any moment.