Gout, with a section on ocular disease in the gouty

by Llewellyn J. Llewellyn

From the above considerations it is, I think, clear that, whatever the hidden nexus between gout and “granular kidney,” it is neither essential nor constant. It is rather, I believe, of the nature of a coincidence. Furthermore, as applies to so many problems pertaining to gout, and, for that matter, to “granular kidney” also, we labour under the grave disability that both terms are, especially “gout,” very vaguely applied and when used are often a matter of personal opinion. Consequently, as Samuel West shrewdly observes, “it is difficult to discuss satisfactorily the relation of two conditions to each other when neither condition admits of precise definition, for some authorities are more easily satisfied in the diagnosis of gout than others; and, while some place all forms of chronic interstitial nephritis in one and the same category, others are not so comprehensive, and regard granular kidney as a definite clinical disease, of which the interstitial nephritis is only a part.” Under these circumstances, the need for further and more exact researches in this sphere is but too obvious.

Meanwhile, accepting the general opinion as to the frequency of the co-existence of gout and granular kidney, is there any explanation thereof? For myself, I am inclined to believe that the common overlapping of the two disorders is in large measure due to this, that the factors, i.e., excess in alcohol, overeating, etc., that make for the eruption of gout, are largely identical with those that promote the development of granular kidney. Hastings Gilford holds “there is very little doubt that syphilis, lead, and gout do not so much originate Bright’s disease as excite it into activity when it already exists in a smouldering or latent condition.”

With this view I feel much in accord, and if to the malign effects of gout be superadded the effects of alcohol or, haply, lead also, how incalculably greater the chances of fanning into flame any latent tendency to nephritis—a legacy, perhaps, of some long bygone infection.

Prognosis in Gout

Gout per se rarely, if ever, proves fatal. Certainly, as Sir Thomas Watson long since said, “gout in the extremities is not a mortal disease.” When death did occur during or in close relation to an acute paroxysm, it was by our forefathers attributed either to its retrocession or to some misplaced or irregular manifestation. Indeed, their attitude was very much that of the French physician who observed: “La goutte articulaire est celle dont on est malade, et la goutte interne est celle dont on meurt.”

But, as we shall see later in our chapter on Irregular Gout, most, if not all, of their instances of the assumed translation of the materies morbi of gout to some vital organ are without foundation. The demise, often dramatically sudden, was not due to gout, but to some insidious, unguessed-at organic degeneration, or to one of the accidental intercurrent maladies to which these subjects seem especially liable. To sum up, the immediate danger to life from regular gout when uncomplicated is slight.

Not that gout is salutary, lessens the liability to other diseases, or promotes longevity. Very much the reverse—“a tendency to recurrence is a law of the disease.” Broadly speaking, the more pronounced the tendency to recurrence of articular outbreaks, the more protracted the isolated paroxysms, the worse the outlook, the more sombre, too, the greater the number of joints involved. Conversely, if the disease, though it recur, restrict itself to the classic site, the big toe, the longer, as a rule, the intervals of freedom, the brighter the prospects of long life. Lastly, the more the subject is crippled, the more pronounced the tendency to tophaceous deposits, the more likely is the disease to pursue a downward course, the greater the risk of associated degenerations in renal and vascular tissues.

While these reflections are in the main, we think, justifiable, we must recollect that in gout, as in other maladies, the elements of prognosis reside in the individual, not the disease. Does he come of a long-lived stock?—not uncommonly a feature of gouty families. If so, the outlook is favourable. If he come of a short-lived breed, then in all probability, no matter how carefully he lives, he will not likely make “old bones,” this, certainly, if the gout makes its appearance early in life, say under thirty.

As to the axiom, generally accepted, that the earlier in life gout makes its début, the more unfavourable the outlook, there are exceptions. Where longevity marks the stock, they usually are true to type. Thus, even if the first outbreak occurs in the twenties, I have known them reach the allotted span and over. Nor if their urine show traces of albumen is this necessarily of grave import, for these gouty veterans may for many years, even to old age, exhibit traces of albumen without apparently developing genuine Bright’s disease.

“There dies not above one of a thousand of the gout, although I believe that more die gouty,” wrote Graunt long years since; and this contains a kernel of truth, for the prognosis of gout rests in the main not on the gout, but the conditions correlated therewith—the absence or not of complications. For, be it always remembered, gout, though it may appear in youth, is chiefly an appanage of the middle and later decades, in short of the regressive period of life.