Gout, with a section on ocular disease in the gouty

by Llewellyn J. Llewellyn

Garrod again tells us that he saw an initial attack of gout supervene after extraction of a tooth, a sequence attributed by him to loss of blood. How interesting this, in light of the fact that exacerbations of joint disease have frequently been seen to follow the removal of septic teeth. The same authority also noted the incidence of a primary attack of gout following epistaxis, and the same after copious hæmatemesis, and Todd several times observed such articular outbreaks after venesection.

Lastly, says Garrod, “cases illustrative of the effects of the suppression of an habitual hæmorrhoidal discharge are by no means uncommon, and ... numerous instances arising from boils and carbuncles have come under my notice.” By Garrod and his contemporaries all these various determinants of gouty paroxysms, i.e., loss of blood, etc., were believed to exert their influence viâ the nervous system, with consequent disturbed equilibrium of nutritive processes throughout the body. But while it may be admitted that depression of the vis resistantiæ plays a part, it does so, I believe, by favouring the occurrence of infection.

Let us turn now to modern findings, and we shall see that they do but confirm those of the older clinicians. Lambert in 125 cases of gout found the teeth unsound in 82 per cent. of males and 1 per cent. of females, while in 9 per cent. of the former and 17 per cent. of the latter there was associated chronic dyspepsia. Two years after (1909) Wynn, Wirgman and Turner noted the invariable correlation of gout with local foci of infection. In the majority, pyorrhœa alveolaris was present. Tonsillar sepsis, too, was not uncommon, and much more rarely nasal disorders. Again, out of fifty-two examples of so-called “gouty” throat Edward McCracken found pyorrhœa alveolaris to be present in thirty-nine, and Fenner also tells us that this affection is common in the subjects of gout.

In truth, the victims of gouty arthritis are no more immune from dental lesions than those of other types of joint disease. Thus, Mr. Macdonald, dental surgeon to the Royal Mineral Water Hospital, Bath, informs me that this form of oral sepsis is extremely common in gouty individuals, and in my experience it is but rarely that evidences of its presence are not forthcoming in these subjects. The desirability of early recognition of such foci—in light of their highly probable etiological significance—can scarcely be overestimated. For their consequences, both local and remote, are of paramount importance.

Thus, G. I. Stewart’s recent observations have conclusively demonstrated that “bad teeth” are causally related to tonsillar affections. How illumining this, in view of McCracken’s experiences in “gouty throats.” As we saw, pyorrhœa alveolaris was present in more than half the examples. But, more pertinently to the point at issue, he comments on the frequency with which the victims of gout develop acute tonsillitis, of lacunar or parenchymatous type, also that such attacks frequently precede outbreaks of arthritic gout. Duckworth again noted the same liability of the gouty to unsound teeth and tonsillitis, and that the latter was often followed by articular outbreaks. Luff also observed that “gouty” tonsillitis was occasionally a precursor of articular gout, always subsiding on the appearance of the latter complication.

Again, acute and chronic pharyngitis are proverbially common in “gouty” subjects. Moreover, in both types the subsidence of the throat affection has frequently been signalised by an articular outbreak of classic site. Parotitis, too, has been repeatedly met with in gout, and, according to Luff, “rapidly subsides on the appearance of regular gout in one or more joints.”

In truth, whether we peruse recent or older works on gout, we cannot fail to remark the unanimity of opinion as to the frequency of incidence of these glandular affections—these states of oral sepsis—in the subjects of gout. Equally noteworthy is their insistence on the constancy with which such local affections have proved harbingers of oncoming articular outbreaks. Lastly, the mere fact that our forefathers dignified these local disorders with special appellations, “gouty” tonsillitis, pharyngitis, etc., is cogent proof that they regarded them as among the integral features of gout.

Now, as to the true significance of these acute glandular affections, held by clinicians of repute to be of “gouty” origin. What of “gouty” tonsillitis, pharyngitis, etc.? Still more, what of our deductions regarding the relationship of these same when met with in association with other joint disorders? Do we not hold them each and all as evidences of infection—“acute rheumatism,” “gonorrhœal arthritis,” etc.?—and we may well ask, Why not in gout?

Says Duckworth, “Angina tonsillaris—very painful but not suppurating—may in the gouty suddenly yield to an acute articular attack.” Is it not here more than likely that the tonsil was the initial site or portal of infection, and the arthritis secondary thereto? Is not this same interpretation in all probability true also of all forms of “gouty” throats when followed by arthritic outbreaks?

The marvel, then, is that not only have we held, but apparently many still hold, that the tonsillitis, pharyngitis, even the gingivitis—like the subsequent articular lesions—are one and all attributable to the underlying gout. We certainly would not do so in the case of any arthritis other than “gouty,” and to my mind the time is ripe for a change of attitude. The “gouty” throats, like the “gouty” teeth, should be regarded not as symptomatic of gout, but etiologically related thereto. We should cease to talk of “gouty” throats, teeth, etc., should renounce the prefix, for there is nothing specific of gout either in the tonsillar, pharyngeal, or dental lesions. We should instead view these various local disorders in their true perspective as foci of infection, causally related to the subsequent and secondary “gouty” arthritis.