Gout, with a section on ocular disease in the gouty

by Llewellyn J. Llewellyn

Again, as our criteria fall short of identifying the exact form of the “purin combinations” it follows, therefore, that they tell us nothing as to whether “the increase is due to a more active transport of purins from one organ to another for further metabolism or simply to a transport to the kidneys for elimination.”

In other words, hampered by the above disabilities in our tests, it is beyond our power to determine whether “the increases denote a supernormal nuclein metabolism or an unusual type of nuclein cleavage.” Should it ultimately transpire that the increase in the purin blood content is a real one, viz., made up of “an excess of normally formed and normally bound purins,” a great step forward will have been achieved. For, to account for the same it will, as Walker Hall observed, be necessary to postulate a supernormal nuclear activity of generalised or localised distribution.

Need for Further Investigations.—While none can doubt that, by means of chemical investigation of the blood, the clinical problem of gout will be elucidated to a much greater extent than has been possible by means of urine analysis, still much remains to be done before recent findings can be applied to the solution of the etiology of gout.

The results of blood analyses up to now have afforded us no clue as to the intimate nature of the warp in nuclein metabolism. At the most, the researches in this sphere do but make it increasingly clear that uricæmia is not the cause but the result of gout.

Albeit, this conclusion does not justify us in putting out of court all thought of uric acid in connection with gout. Any tendency thereto will be immediately checked when we recall that uratic deposits, i.e., tophi constitute the solitary unequivocal token of gout, and to this aspect of the question the ensuing chapter will be devoted.

Meanwhile, systematic investigations of the purin content of the blood, not only in gouty but in normal subjects, would surely dissipate much of the obscurity that envelops this complex question. It were well, too, that blood and urine analyses go hand in hand in our investigations. How illumining these have been in connection with atophan, the increased urinary output of uric acid having been found to be correlated with a simultaneous sinking in the level of the uric acid of the blood.

Again, the excretion of urinary purin ebbs and flows with the intake of food and the degree of muscular activity, while sleep also exerts an influence, not to mention constitutional disturbances, e.g., fever infections, etc.

Can it be doubted that the blood content of uric acid varies with these same vicissitudes? Walker Hall tells us that the data to hand, “as to the rapidity of the appearance of purins in the blood-stream after food, infections, fever, etc.,” though few in number, yet suggest that “the excretion by the kidney is tidal in character, and that the blood uric acid has similar characteristics.” In light of these possibilities, we may well pause before attempting to appraise exactly the significance of isolated blood examinations.

What, too, as the above authority observes, of the influence on the gouty uricæmia of infancy, puberty, the menopause, and for that matter the pre-senile and senile periods of life with their associated vascular lesions? The researches of Uffenheimer prove that even in young children the disorders of purin metabolism distinctive of gout are to be met with, i.e., “infantile gout.”

We stand also in urgent need of knowledge as to the uric acid blood content in the early as opposed to the late stages of gout; in need, too, of further examinations of the blood to this end, not only during the passage of acute attacks, but even more under those conditions which are presumed to determine their incidence.