But, despite these gaps in knowledge, these disabilities of technique, there is no need for despair. “It is a slow progress along the zigzag which leads to the centre of the ‘gouty maze,’ but the researches of the last decade have opened up many new and possible pathways thereto.”
CHAPTER XII
URATOSIS IN RELATION TO GOUT
The two salient features of the gouty diathesis are:—
(a) The tendency to excess of uric acid in the blood, i.e., hyper-uricæmia, and
(b) The tendency to uratic deposition, i.e., uratosis.
With the former we have dealt, but before passing to discuss the latter, it will, we think, be advisable to review both these morbid tendencies in relation to gout.
Hyper-uricæmia and uratosis, though they both occur in gout, are by no means of identical pathological valency or significance. In hyper-uricæmia the uric acid, either in a free state or combined, circulates in the blood and lymph. In uratosis the uric acid is anchored in solid form in the substance of the tissues. In the former, then, the uric acid, if it be noxious, acts as a chemical poison, in the latter as a mechanical irritant.
But the more striking contrast is that while hyper-uricæmia is not restricted to gout, but occurs in many other disorders; on the other hand, uratosis is absolutely confined to the gouty state, constituting its pathognomonic stigma.
Again, hyper-uricæmia may exist for prolonged periods without producing uratosis. But uratosis cannot, as far as is ascertained, occur without a co-existing hyper-uricæmia. From these disparities it may legitimately be inferred that the factors responsible for the genesis of hyper-uricæmia and of uratosis, are not identical; in other words, that in uratosis some other agency or agencies are at work over and beyond those that beget hyper-uricæmia.