Gout, with a section on ocular disease in the gouty

by Llewellyn J. Llewellyn

The question then arises, Is gout haply due to a retention of other metabolites? That outbreaks of gout follow fast on the heels of dietetic irregularities is proverbially true. But there is no certain evidence that the symptoms generally ascribed to auto-toxæmia are referable to substances derived from the foodstuffs under the action of the digestive juices. Toxic as are peptones and primary proteoses when they gain direct access to the tissues, the symptoms produced in no way resemble those affiliated to alimentary toxæmia, much less those of gout. Rather, according to Adami, do they approximate to those typical of anaphylactic shock.

Normally, too, the mucous membrane proves an efficient barrier, these poisonous bodies during their passage through it being transmuted into harmless substances. Nor can we refer the symptoms of gout to a toxæmia secondary to intestinal stasis or other causes. In other words, it cannot be attributed to assumed toxic action on the part of the intermediary and terminal products of protein disintegration. For seemingly these chemical outcasts of the economy become progressively less toxic on their downward path to effete matter.

The diamines, too, produced by bacterial action on foodstuffs, are so minimal as to be negligible, while the toxicity of cholin and neurin is unestablished; and as for indol and skatol, they are with difficulty absorbed from the healthy colon. Experimental researches on carbohydrate and fatty disintegration have likewise proved sterile, while there is no evidence that the anaerobes present in the digestive tract produce ecto-toxins, or undergo lysis with release and absorption of their endo-toxins.

In short, it is but too clear from the foregoing brief résumé of recent experimental findings that, if uric acid cannot be held responsible for the causation of gout, there is no evidence likewise that the disorder owes its genesis to any other of the as yet isolated chemical products of gastro-intestinal digestive activities. Having dealt with this aspect of the question, we shall now pass on to consider whether the phenomena of gout can be more adequately explained on a basis of infection or sub-infection.

Infection or Sub-infection.—Our knowledge as to the exact manner in which local foci of infection work their malign effects almost daily undergoes expansion. It will be recalled that Stewart has shown that “bad teeth” are often etiologically responsible for tonsillar inflammation. It further is well established that streptococci are of common incidence in the tonsils, and Rosenow and Brown from experimental observation have established that these hemolysing organisms, migrating viâ the blood stream, exhibit a marked predilection for forming a fresh nidus in the gall bladder. Here they may initiate a cholecystitis, and secondly gallstones, and in sequence thereto the symptoms associated with gall-bladder-dyspepsia. The same formidable list of sequels may follow infection of the gall bladder from the teeth, stomach, or intestines, notably from the vermiform appendix.

In like fashion the origin of appendicitis may be traced back to septic foci in the mouth, tonsils, naso-pharynx, or to the gastro-intestinal tract. Here again there ensue the symptoms of so-called appendix-dyspepsia. As in the case of the gall-bladder variety, the primary lesion in the appendix may be latent, and the exact diagnosis may be a matter of great difficulty, often indeed only to be achieved retrospectively, viz., when abatement of the symptoms follows ablation of the appendix.

We see, therefore, how far-reaching are the consequences of local foci of infection in the mouth or elsewhere. Now, the gouty subject enjoys no immunity from the remote sequels of local sepsis. But as a rule, unfortunately, whatever be the nature of his dyspeptic symptoms, they are, like his dental anomalies, his tonsillar inflammations, forthwith dismissed as symptomatic of gout, not etiologically related thereto.

Now, I have seen pyorrhœa and chronic appendix-dyspepsia running side by side in the same subject with recurring classical attacks of gout in the big toe. The faulty teeth were extracted, and later the chronically inflamed appendix removed; and though he had an attack of gout shortly after the operation, there has as yet been no recurrence thereof.

Again, by the older writers “gout in the liver” was most firmly believed in—as one authority puts it, “a subacute catarrh of the intrahepatic biliary system which may lead to a subacute parenchymatous hepatitis”! But more pertinent to my point is the insistence of older authors upon the frequent association of gout and gall-stones. Senac, of Vichy, claimed indeed that out of 166 cases of biliary lithiasis 95 had gout or an hereditary predisposition thereto. Judging by modern experience, this is probably a gross over-estimate. In contrast, our own countryman Murchison dwelt upon the frequency of jaundice in gout independently of biliary colic. And, as we shall see later, Brinton held that many of the dramatic phenomena accredited to “retrocedent gout” were unrecognised examples of biliary colic.

But, controversy aside, the point I would lay stress on is, that we should refrain from labelling offhand “dyspeptic” symptoms in a “gouty” subject as gouty, this when we are so constantly confronted with local foci of infection in the mouth, or elsewhere, which afford us an explanation of the gastro-intestinal symptoms at once more obvious and more rational. This also the more especially in that—as far as subjective symptoms go—those deemed typical of so-called “gouty” dyspepsia are indistinguishable from those met with in appendix- or gall-bladder-dyspepsia. Indeed, I might go further and point out that the variations in free HCL in the gastric juice—as observed in gout—conform to those met with in the above disorders. Thus, in “gouty” dyspepsia, the free HCL may be normal, in excess, or wholly absent, as in gall-bladder or appendix-dyspepsia. I would therefore plead that in any “dyspepsia” arising in a genuinely gouty subject we endeavour to elucidate the exact nature of the underlying lesion, but to this we shall return again when discussing diagnosis.