URIC ACID IN RELATION TO GOUT It will be recalled that at the close of our chapter on Pathogenesis we referred to the growing scepticism of Garrod’s views as to the pathogeny of gout. Still, if we except Edward Liveing’s pertinent observation that _uricæmia_ was not peculiar to gout, naught, save alternative hypotheses, unsupported by pathological data, was advanced. Consequently, Garrod’s facts never being seriously called in question, his position remained unassailable, until, in the year 1898, his original observations as to the lowered alkalinity of the blood in acute gout, and the increased uric acid content thereof during the same, were definitely contradicted by Magnus Levy. Working with more modern and more reliable methods of technique, this observer, in a series of seventeen cases of acute gout, found no evidence of any lessening in alkalinity of the blood or of any augmentation of its uric acid content as compared with the inter-paroxysmal period. Again, as to Garrod’s claim that there was a diminished excretion of uric acid during the attack, this also, while supported by Minkowski, was called in question by Pfeiffer, Levy, and Badt, who found the reverse to be the case, _i.e._, a notable increase in the excretion of uric acid during the paroxysm. These results were again in 1900 confirmed by Chalmers Watson. An exhaustive study of a series of cases of _acute gouty polyarthritis_ convinced him that:— (1) The alkalinity of the blood is not diminished during the attack. (2) The excretion of uric acid is not lessened during the paroxysm, but the reverse; there is, therefore, no ground for the supposition that there is a temporary diminution in the capacity of the kidneys to excrete uric acid. (3) The amount of the uric acid in the blood is not greater during the attack than in the intervening period, and if these points be accepted, we must start _de novo_ in search of the cause of the acute paroxysm. The iconoclastic revelations of the foregoing researches may well form a preface to our discussion of gout from the triple aspect of:— (1) Uric acid excretion. (2) Uricæmia. (3) Uratosis. URIC ACID EXCRETION IN GOUT The earlier investigations as to the behaviour of uric acid in the organism were necessarily restricted to the noting of any variations in the uric acid output in the urine. That the findings and, alike, the deductions proved bewilderingly contradictory is not to be marvelled at when we recall the many factors that govern the amount of uric acid excreted in the urine.