Gout, with a section on ocular disease in the gouty

by Llewellyn J. Llewellyn

We know that, given oral sepsis, sequential infections of the appendix and gall bladder are not uncommon. Recently it has been remarked that many gouty patients suffer with attacks of pain in the region of the appendix, and simultaneously tenderness over the gall bladder. That the subjects of gout enjoy no immunity from appendix or gall bladder disorders is certain, and at this we need not be surprised, seeing the frequency with which they suffer from alleged causes thereof, i.e., dental sepsis, etc.

But what we would insist upon is that we should not be content merely with dubbing these symptoms “gouty,” as they are much more likely to be, not symptomatic of gout, but etiologically related thereto. If then we are to arrive at the exact nature of the underlying lesion, the probable site of infection or toxic absorption, we must invoke all modern methods of investigation. Thus, how valuable the existence of an X-ray barium or bismuth meal in furnishing positive evidence of gastric or duodenal ulcer on the one hand or of gall bladder or appendix disease on the other. What an aid to the location of adhesions the demonstration of ileal and cæcal stasis, etc.!

In obscure cases the fæces may have to be scrutinised for evidences of pancreatic inefficiency, viz., bulky pale stools, undigested meat fibres, and excess of neutral fat. Their bacterial content, too, if abnormally high, should be noted. As in other arthritides of unknown origin, the results following the administration of vaccines prepared from the predominant organisms have been such as to suggest a causal connection.

The urine should be subjected to chemical and bacteriological examination. As to uric acid, the delusion still widely prevails that gouty subjects excrete large amounts thereof. How frequently is “the degree of acidity” of the urine or “its content of uric acid” held to justify a diagnosis of gout. The deduction is quite unjustifiable. Equally so the assumption that the reverse, a defective excretion of uric acid, is an invariable feature of the gouty diathesis. For though when on a purin-free diet the output of uric acid in the gouty is low, it rarely, if ever, falls below the level of normal. The truth is that we cannot on the mere basis of the variations in uric acid excretion in the urine presume to diagnose gout.

To have any semblance of diagnostic value, the patient should be on a purin-free diet, and a long series of exact quantitative examinations made. C. v. Noorden, to gauge the limit of tolerance of his patients, gives them increasing amounts of purin, and so determines the quantity the subject can deal with without showing retention. But, as Von Fürth satirically observes, “when a physician allows a quantitative analysis to be made of any arbitrarily collected specimen of urine of his patient and then makes a diagnosis of the presence or absence of a ‘gouty diathesis’ after a glance at the list of data of the analysis, he is really not proving by his actions his possession of diagnostic acumen as much as he is laying bare his total ignorance of bio-chemical matters.”

So much for the diagnostic valency of uric acid estimates in chronic gout, but if the patient be on purin-free diet, and an acute attack ensue, the curve of uric acid excretion is fairly characteristic. In other words, for a day or two preceding the outbreak, the uric acid output falls below the usual level, but early in the attack rises markedly, to be followed by a secondary fall.

Some aid in diagnosis has been afforded by the fact that after ingestion of purin-containing food the gouty individual does not, like a normal person, eliminate the excess of uric acid, but the excretion is “spread out over a number of days.” But this retardation and diminution in the excretion of exogenous purins has been seen in non-gouty forms of arthritis, not to mention some cases of nephritis and chronic alcoholism. Hence delayed nuclein exchange, though highly suggestive of gout, is not infallibly diagnostic thereof.

As to uric acid in the blood, it will, I fear, not for long, if ever, be easy to prevail on patients to submit to withdrawal of the amount of blood necessary, even by modern methods, for its estimation. Fortunately, our American confrères appear to be more successful in securing such opportunities. Pratt states that in his twenty-one cases of genuine gout the uric acid content of the blood, irrespective of diet, was 3·7 mg. per 100 grams, as opposed to 1·7 mg., the average amount in 156 non-gouty cases studied by Adler and Ragle. Still Pratt noted that in a few cases of undoubted gout the uric acid content of the blood was within normal limits, though it never fell, even on a purin-free diet, below 1·4 mg. Nevertheless he holds that there is conclusive evidence that the uric acid content of the blood is in gouty individuals notably increased both in the intervals and during attacks.

He has found the sweetbread meal an aid in diagnosis, and the following is his method of procedure: “The patient is placed on a purin-free diet, and the daily output of uric acid in the urine determined. After having been on this diet for at least four days the blood is analysed for uric acid, and 150 to 300 grams of sweetbread (weighed raw) are fed. The purin-free diet is then resumed. The blood of gouty subjects forty-eight to seventy-two hours after the sweetbread meal has shown in every case examined an abnormally high amount of uric acid, while in control subjects this was not found. It is not improbable that this rise in the uric acid content of the blood may occur in certain cases of nephritis and other pathological conditions.”

A bacteriological examination of the urine should be undertaken. Trautner held mucous colitis as one of the initial manifestations of gout, and believes that the bacillus coli communis is the primary agent in gouty affections. He suggests that it produces a reducing substance which during its passage through the body is transmuted into xanthin and uric acid. Be this as it may, there is increasing evidence that an etiological potency may attach to coliform bacilli, streptococci, and other organisms. Dr. Munro in his researches at the Royal Mineral Water Hospital, Bath, noted that the blood serum in one of my cases of acute gout agglutinated B. coli. He has also found streptococci in the urine in acute gout, and these subjects certainly enjoy no immunity from other forms of bacteriuria.