(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.
How fallacious, it now transpires, were the assumptions based upon the mere uric acid output in the urine, and how little understood even to-day the many conditions that determine its variations.[17] But, fortunately, we can now to some extent control and review our urinary findings in light of the uric acid content of the blood. But we anticipate, and meanwhile let us confine our discussion to the variations in uric acid excretion that occur in gout, and this as revealed by more modern students of the disease. This will be more conveniently dealt with if we consider first the oscillations in uric acid output in relation to acute attacks of the disorder, and subsequently the same as met with in its more chronic manifestations.
Uric Acid Variations in Acute Gout
Generally speaking, there appears to be a consensus of opinion on the following points:—