Gout, with a section on ocular disease in the gouty

by Llewellyn J. Llewellyn

Our dietetic ventures must obviously rest on a sounder basis. This we do know, viz., that functional disturbances of digestion generally precede a “gouty” paroxysm, and that their amelioration is followed by relief of symptoms. The aim of our dietetic measures then is the prevention of digestive disturbances, not the routine withdrawal or reduction of uric acid precursors.

The dietetic treatment of the “gouty” is that of the “dyspeptic,” with, if anything, an added discrimination, for an unknown factor intrudes—the “gouty diathesis”—which has also to be reckoned with, but of this later. Now “dyspeptics” cannot be dieted by rule of thumb. Whether they be “gouty” or “non-gouty” matters not. A careful study of the phenomena of digestion, if not essential in every case, is certainly called for in the more obstinate and obscure forms. In short, an attempt should be made to determine the special form of “indigestion.” Is the derangement of function a disorder of motility or secretion? Is it catarrhal or nervous in origin?

That such is the proper mode of procedure is undeniable. For are we not too prone to assume that the “dyspepsias” of the “gouty” are sui generis, all due to one cause, the materies morbi of gout, instead of being merely “excitants” of gout and due to a variety of digestive functional disabilities, and these of equally diverse origin?

Thorough Physical Examination a Necessary Prelude to Dieting.—When we recall that the “dyspepsias” of the “gouty” endure through long years, the suggestion that every effort should be made to localise and establish the exact nature of the underlying derangement seems almost superfluous. Yet how often is the question dealt with offhand, though, ideally speaking, I cannot help thinking that the primary outbreak of gout should be the signal for an exhaustive examination by all modern methods. The consequences of dyspepsia in the “non-gouty” are bad enough, but infinitely more so in the “gouty” subject. But it is the former group, not the latter, that has been the favoured object of study by experts, which is, I think, somewhat unfair.

There is need of a searching investigation, a more common invoking of the tests whereby the functional efficiency of the stomach may be gauged. We know that there may exist on the one hand hyperchlorhydria and on the other hypochlorhydria. But we need to know more as to disturbances in gastric motility, delay or hurry in digestion, not to mention abnormalities in shape, position, size, tone, pyloric end rhythm, etc. In view of the almost general admission that gastro-intestinal derangements are causally related to outbreaks of gouty arthritis, surely our remissness in this matter is somewhat surprising, the more so in light of the heroic procedures, viz., ileocolostomy and colectomy, advocated in rheumatoid arthritis, a condition by many deemed related to gout.

Leaving such aside, none will, I think, deny not only the value of test meals for free HCL variations and experimentation with all kinds of foodstuffs, but also of X-ray examination of the alimentary tract. How subversive of all preconceptions the revelations of radiography in gastric and intestinal conditions, of what infinite value in disentangling the ambiguous significance of purely subjective sensations! Thus, alterations in gastric tone, motility, and peristalsis may hark back to remote lesions in gall bladder or appendix, and these also account for variations in free HCL.

“Great eaters,” said Sydenham, “are liable to gout, and of these the costive more especially”—an observation the truth of which all will confirm. It may be taken as a maxim that nothing for the gouty is more prejudicial than constipation. Here it is obviously of importance that we know the site of delay, whether in the lower coils of the ileum, the colon, or merely the rectum, i.e., dyschezia. How else obtain this information, save through X-ray examination?

Any departure from normal in consistency, colour or content of the fæces should be noted so as to identify hepatic or pancreatic derangements. An analysis of the urine should always be undertaken, its reaction noted, the presence of albumen or casts ascertained. It is important, too, that we do not overlook glycosuria or oxaluria, or substances indicative of excessive intestinal putrefaction. All these bear far more pertinently on diet than estimates of uric acid.

The behaviour of the skin, whether inactive or not, must also be taken into consideration. Moreover, as the subjects of gout are usually middle-aged or old, it is highly important to note the general drift of metabolism, whether in the direction of obesity or undue leanness. Herewith we must take an inventory, as it were, of the subject’s general mode of living. What are his habits in respect of food and drink? Is his diet excessive or improper in quality? Are his meals taken at irregular times? Does he masticate his food properly?

In the matter of exercise, his occupation or pursuits require thought. Do they involve excessive exertion or favour a sedentary habit? For both these factors bear narrowly on his power or not of disposing of ingested material. Indeed, all the foregoing reflections stand in close relationship to the complex processes of digestion and metabolism, and the efficacy of our prescribed regime will depend on how far our suggested innovations meet the particular needs of the subject under review.