Local Foci of Infection
The extreme frequency with which infective foci are met with in the victims of gout is by no means adequately realised. Moreover, we are only now beginning to appreciate the grave significance of such “nests” of infection and how devious are the ways in which they work their malign influence. For our forefathers gout began, and, forsooth, often ended, in the “stomach,” or it was the “liver” that was impeached. But the portal to the alimentary canal was for them only a cavity, the contained structures of which, albeit, to their mind often betrayed evidences of a “gouty diathesis.” They distinguished “gouty” teeth, “gouty” tonsillitis, “gouty” pharyngitis, even “gouty” parotitis; but all these they classed as tokens or sequelæ of gout—not possible causes or excitants thereof.
Nevertheless, their observations on “gouty” teeth are of deep interest, though their significance was misinterpreted.
Thus, Duckworth, for example, wrote: “The tendency to shed sound teeth has been noted with some frequency in middle or later life in goutily disposed persons, and they are more than others liable to occasional and fugitive attacks of pain in several sound teeth at a time, with a sensation as if these were starting from their sockets, being tender to bite upon.” In truth, a succinct picture of pyorrhœa alveolaris, of unprejudiced source, hence the more valuable.
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.
Gastro-Intestinal Disorders.—It is a matter of common experience that acute attacks of gout are often preceded by or associated with flatulence, heartburn, acidity, loss of appetite, confined bowels, scanty, high-coloured urine, and a feeling of lassitude. In short, nothing is more certain than that exacerbations or relapses very commonly follow symptoms referable to gastro-intestinal and hepatic disorders.
How well established is it that these subjects after unusual, though not necessarily excessive, indulgence at the table, almost inevitably, and sometimes almost immediately, suffer twinges in the big toe, if not frank outbreaks of gout. Such reaction seems to indicate clearly that the functional disturbances in the alimentary tract stand in some causal relation to the subsequent arthritic phenomena. The assumption gains colour, too, from the very certainty with which freedom from such gouty manifestations is attained by abstinence from, or more moderate indulgence in, articles of diet predisposing to such ebullitions.
So much by way of prelude as to the probability—attested by clinical observation and the results of treatment—that the intestinal canal is often the source of the responsible microbe or toxin. Let us now pass to consider what factors other than an oral sepsis may favour the incidence of functional disorders of the alimentary tract.
Variations in Free HCL.—Some years ago Grübe and Falkenstein found that in gout the hydrochloric acid of the gastric juice, far from being increased, was in most cases diminished or wholly wanting.
Now, as we know, the gastric juice when of normal acidity is quite capable of dealing with moderate quantities of pathogenic bacteria. But in the presence of oral sepsis it is probable that a greater number are swallowed than can be satisfactorily coped with.
Given therefore excess of pathogenic organisms and relative insufficiency of free HCL, conditions favourable to the growth of bacteria ensue, while incidentally the chance of such reaching the intestine is materially enhanced.
When, however, the defensive barrier is wholly withdrawn, viz. when there is an absence of free HCL, then of course the necessary inhibition of microbic growth fails of achievement. Moreover, also owing to diminished acidity, ill-digested protein substances gain access to the intestine, and their subsequent putrefaction is favoured.
In opposition to the foregoing, many hold that an excess of free HCL in gout is not uncommon, and unquestionably some are thus troubled. The pernicious effects of the hyperchlorhydria are accentuated by the fact that intestinal indigestion ensues secondarily, owing to the acid chyme completely antagonising pancreatic secretion and thus impairing digestive capacity.
Intestinal rather than gastric indigestion is, I think, more typical of the gouty subject. It will be recalled that the food nucleins are unaffected by the gastric juice, and though the protein moiety is split off from the nucleinic acid by the pancreatic ferments, yet neither the poly- nor the mono-nucleotides are thereby acted upon. It is in truth the succus entericus with its nucleotidase that plays the most important digestive rôle as regards nucleins, breaking them up into nucleosides which are, to a large extent, absorbed as such.
To resume, this condition of intestinal indigestion may arise from a variety of causes: excess or deficiency of gastric juice, defective motility, and diminished secretion of intestinal juices, and in all cases improper food may determine such intestinal derangement.
The clinical features presented are very variable. It is often difficult, if not impossible, on the basis purely of the subjective symptoms, to decide in any given instance how far the symptoms are referable to intestinal stasis, or to a chronic infection, with a resultant catarrhal state of the mucosa, or to both causes combined in varying proportions.
But, be the explanation what it may, in our experience the most common antecedent or concomitant of gout is intestinal dyspepsia. Its secondary consequences are far reaching, especially if the small bowel be involved, catarrh of which may lead to reduction in the secretion of bile and pancreatic juice.
How commonly in these cases do we meet with symptoms indicative of sluggishness of the hepatic functions, such as turbidity of the urine, a pale or abnormally dark colour of the alvine evacuations. Also, whatever be its true etiology, they exhibit not so uncommonly sugar in the urine, the so-called “gouty” glycosuria.
Now, as a mere glance will show, diminution and impairment of the biliary and pancreatic secretions have far-reaching consequences. Foodstuffs undergo abnormal changes, are less easily absorbed, and simultaneously chemical products are formed which irritate the intestinal mucosa. Nor do the baneful effects cease here, for, owing to the unusual nature and reaction of the intestinal content, the bacterial flora in the bowel undergo modifications.
Thus, organisms normally present only in small numbers in the small intestine find the altered medium more suitable for their growth and multiplication; while others, whose usual habitat is the large bowel, migrate upwards, and infect the ileum and duodenum, and ultimately the biliary and pancreatic passages.
In the presence of such deficiency in the intestinal juices, proteins are imperfectly digested, and putrefaction under microbic action favoured. At the same time the digestion of carbohydrates is impaired, organic acids are formed, and gases in larger amounts liberated. Ultimately, owing to absorption of these irritating products, a condition of chronic toxæmia results.