Elimination of the Infective Arthritides

Yet again was the territory of gout destined to undergo further restriction, and this largely owing to the rise of the science of bacteriology. For in light of recent improvements in diagnostic methods, who can escape the conviction that under the term “gout” had been wrongfully included many forms of arthritis, now known to be due to specific infections. What, for example, of Hippocrates’ aphorism that gout was unknown in youths—ante usum veneris—who can doubt that some of his reputed cases of gout were examples of gonococcal or syphilitic arthritis?

What, too, of all the other infective arthritides—influenzal, pneumoccocal, scarlatinal, typhoidal, meningococcal—to mention only those actually affiliated to some specific organism. For gout, be it noted, confers no exemption from other arthritic diseases, but how in time past were such to be differentiated therefrom?

Again, gouty subjects, as has been recently emphasised, are notoriously prone to pyorrhœa alveolaris, and how difficult, given the supervention of an arthritis in such to define the causal agent—gout or sepsis, which? Small wonder then, that the clinical content of gout, not only to ancient, but also to latter day physicians, loomed large, swollen as it undoubtedly was by the inclusion of infective arthritides, not to mention those of traumatic or static origin.

That more of these alien joint disorders—les pseudo-rheumatismes infectieux, as M. Bouchard terms them, were relegated to the “rheumatic” than to the “gouty” category, may perhaps be allowed, but still gout was undoubtedly allotted its full share and to boot. Moreover, if to “rheumatism” was wrongly affiliated the lion’s share of the infective arthritides, on the other hand to “gout” accrued a host of unrelated visceral disorders, not to mention affections of the nervous and vascular structures, etc.

In endeavouring to summarise the results of our brief retrospect, the somewhat chastening fact emerges, viz., that the isolation of articular gout has been achieved not so much by an increase in our knowledge as to what is gout, but through our growing perception of what is not gout. For of the causa causans of gout we are still as ignorant as in the days of Sydenham. But, in contrast, our enlightenment as to the clinical and pathological features of other forms of arthritis has steadily progressed. In this way, shorn of many alien joint disorders, gouty arthritis has slowly but surely asserted itself as a specific joint affection, distinct both from rheumatism and arthritis deformans.

In the course of our sketch, too, we have traced the evolution of the modern opinion that at least two separate conditions, “rheumatoid arthritis” and “osteoarthritis,” are comprised under arthritis deformans. This most tardily arrived at differentiation has done more than any other to clarify our conceptions as to what constitutes true “gouty arthritis.”

If to this be added the further differentiation, not only of the nerve arthropathies, but also of the infective arthridites—both specific and undifferentiated forms—it will be seen that the term “gouty arthritis,” once the most comprehensive perhaps in all medical nomenclature, has now been brought within, at any rate, reasonable distance of more or less exact definition.

CHAPTER III
EARLIER THEORIES OF PATHOGENESIS

The fanciful views of the humoralists as to the etiology of gout exercised almost undisputed sway up to the latter half of the eighteenth century. At that time the great Scottish physician, Cullen, took up arms against a doctrine which appeared to him unjustifiable in conception and baneful in practice. He inclined to the solidists rather than to the humoralists, claiming that gout was the outcome of a peculiar bodily conformation, and more especially of an affection of the nervous system. While he categorically denied that any materia peccans was the cause of gout, he yet admitted that in prolonged cases a peculiar matter appeared in gouty patients. But, in view of latter day revelations, Cullen, with singular prescience, maintained that the said matter was the effect and not the cause of gout.

Albeit, notwithstanding the almost universal deference accorded to Cullen, his theory, promulgated in 1874, though previously adumbrated by Stahl and afterwards reinforced by Henle, secured but few adherents. The source of this was not far to seek. For ever since the discovery of uric acid by Scheele in 1776, and its detection in tophi by Wollaston, an increasing body of opinion inclined to the view, that in some obscure way the life history of gout was bound up with that of uric acid.

Still, despite able advocacy in this country by Sir Henry Holland, Wollaston, and others, not to mention Continental authorities, such as Cruveilhier, it was felt that scientific proof of the truth of their contention was still lacking. But not for long were they left in doubt. For, in 1848, Sir Alfred Garrod’s momentous and epoch-making discovery of the presence of uric acid in the blood of the victims of gout allayed all doubts, and seemed then and for long after an all-sufficient explanation of the protean manifestations of the disease.

This distinguished physician enunciated his views in a series of propositions which embodied the result of his researches and incidentally laid the foundations of the uric acid theory.