Gout, with a section on ocular disease in the gouty

by Llewellyn J. Llewellyn

Need for Collaboration of Clinician and Bio-chemist.—Before we shall be able to lay down a diet for the “gouty” on truly scientific grounds much remains to be done. Our clinical examinations, in no way to be despised, must nevertheless be supplemented by the more subtle tests of the bio-chemist. Consider the complexity of the problem. We have to diet not only the “gouty,” but the “potentially” gouty.

They shade the one into the other. Even the man who has had gout has his periods of respite, of apparent unblemished health. If seen at such a juncture, he may display the relics of his gouty attacks, i.e., tophi. But can we say of him that he actually now has gout? He has crossed the Rubicon, disclosed his morbid trend, but meanwhile he has apparently recrossed to the vantage ground of normal metabolism. He stands again with those who are about to, but have not yet developed the disorder, i.e., the “potentially” gouty.

Who will deny that it is when a man is, so to speak, gravid with, but not yet delivered of, gout that dietetic measures will avail him most? But this, alas! carries with it as its postulate the diagnosis of latent gout. Now, Walker Hall suggests that “the nuclein metabolism of the gouty patient is run at high pressure or full capacity, instead of the usual normal quarter or at half-pressure capacity, in order to cope with the ordinary processes of assimilation, and that there is very little reserve energy.” Does not this seem to indicate that a fruitful sphere of research might be the invoking of “endurance” tests and other methods of determining the functional capacity or efficiency of the various viscera?

At present we content ourselves with blaming the stomach, the liver, the kidneys, etc., and often on very inadequate grounds. It would be a great step forward if we could determine betimes which particular viscus is functionally deficient. There are signs that this boon will not be long withheld, signs that not only can the functional efficiency of the stomach be tested, but also of the liver, kidneys, and even the spleen.

Thus Labbe and Daughin study the colloidal nitrogen in the urine, and find the ratio to the total nitrogen much augmented when the functional efficiency of the liver is depressed. Again, Bauer and Spiegel use the bilirubin content of the blood to the same end. They maintain that there is a bilirubin threshold, the assessment of which denotes the functional capacity of the liver. In health the blood content thereof is surprisingly uniform. But in passive congestion of the liver it rises very markedly, and the same after administration of cholagogues.

In like fashion the value of blood urea concentration is extolled by Kast and Wardell as a satisfactory index of the functional power of the kidney. The uric acid content of the blood is by Baumann, Hansmann, Davis, and Stevens regarded as a very delicate index of renal function, though unreliable in the presence of œdema, cardiac decompensation, or when the urine is highly concentrated in hot weather. These are but a few of the methods available, and in the same way Frey has devised tests for the functional efficiency of the spleen, while Barton invokes the administration of urea, chlorides, adrenalin, creatine, etc., to assess the functional capacity of the liver, kidney or spleen.

Such is the trend of modern medicine—to link up clinical with laboratory findings—and in gout perhaps more than in any other disease is this collaboration urgently called for. For who can doubt that gout is a malady of mixed intrinsic (endogenetic) and extrinsic (ectogenetic) origin?

We need to know more about the endogenous factor, the basal perversion of cell structure or function, that differentiates the tissues of the “gouty” from those of their fellows. For it is these inherent peculiarities—structural, physical, or chemical—that give to the disease its sui generis character. How then in the “living” subject shall these hidden morbid potentialities be identified? How save through the medium of function, the outward expression of metabolic activities, in other words by appraisement of the functional capacity of the various viscera? For gout primarily is a disorder of function, or, as Rendu phrased it, a primordial “vice of nutrition.” Hence our insistence on the invoking of the various laboratory methods for elucidating the functional powers, the efficiency or not of the liver, kidneys, etc.

This satisfactorily achieved, we may, through their reflected functional disability or disabilities, divine somewhat the nature of the innate tissue peculiarities of the “gouty,” may hope at long last to translate the misty “gouty diathesis” in terms of functional deficiency, deficiency of the working capacities of the stomach, liver, or kidneys, and perhaps find that the basal flaw in some lies in the liver, in others in the kidney, and thus the older clinicians be justified of their claims for “hepatic” or “renal” varieties of gout.