Straightway xanthin, hypoxanthin, adenin, etc., were credited with pernicious potencies.[26] Nor did they lack apparent support from the experimental side. Thus, Mandel affirmed that purin bases, apart from infection, might originate pyrexia. Others, again, noted that in dogs and rabbits fed on adenin, degenerative changes in the kidneys ensued, with deposits resembling uric acid and urates in their substance. The fact, too, that guanin-gout was occasionally met with in swine, also lent colour to their views.
Moreover, that ingestion of these congeners of uric acid led in animals to renal lesions, seemed to support the contention of many, that renal disorder might be the primary cause of gout. But, unfortunately, Kolisch and Weintrand’s assertion that the alloxur bases were found in increased quantities in the urine of gouty patients was contradicted by Schmoll, His, Laquer, and others.
Still more cogent, apparently, the announcement in 1910, by Brugsch and Mallory, that they had seen a typical attack of gout ensue in a gouty patient in sequence to a dose of 0·5 gram of hypoxanthin. Nor did this reaction of gouty persons fail of confirmation, as in the same year, Brugsch and Schittenhelm, in gouty patients, noted attacks of arthritis, after the administration of nucleinic acid.
Nevertheless, we must beware of laying too much stress on isolated experiments of this nature, so hypersensitive are some of the victims to any strange or unaccustomed ingesta. Were all the myriad other determinants of gouty attacks eliminated, over-drinking, trauma, mental disturbances, etc.? for be it recollected, all the victims of these experiments with hypoxanthin and nucleinic acid were gouty subjects, i.e., potentially liable to attacks at any moment.
Even admitting the ingestion of, e.g., hypoxanthin was followed by a gouty outbreak, it must be insisted that mere sequence does not establish causation. Clinically, on the whole, there is little or nothing to support the contention that the purin bases have much to do with the pathogeny of gout. “The proof of the pudding is in the eating,” and contrary to the view, at one time so prevalent, that purin foodstuffs were most deleterious, it has been found that, for the average gouty person, a purin-free dietary is not only not essential, but prejudicial. Those, therefore, who may be inclined to see in the above sequence proof of a causal connection, would do well to recall Bacon’s dictum that “there is in the human mind a peculiar tendency to dwell on affirmative and to overlook negative instances.”
In conclusion, we must affirm our belief that neither uric acid nor its precursors is responsible for the fever, local inflammation, and general constitutional disturbance in gout, for uric acid and the urates are themselves practically non-toxic. Albeit, though holding this view, I do not for one moment suggest that uric acid has nothing whatever to do with gout. The fact that tophi, its pathognomonic stigmata, are compounded of biurate of soda, would per se stamp such an attitude as untenable. On the other hand, uric acid must be viewed in its proper perspective as a concomitant or sequel of gout, the essential cause of which must be sought elsewhere.
CHAPTER XIII
THE RISE OF THE INFECTIVE THEORY
With the abandonment of the uric acid theory of the causation of gout we see a reversion, curiously enough, to the hypothesis held by the ancient physicians as to its pathogeny. Like Cælius Aurelianus and Paulus Ægineta, we now incline to refer the origin of the disorder to some derangement of the gastro-intestinal tract. This conception indeed endured up to the latter half of the eighteenth century, and was definitely maintained by Van Swieten in his commentary on the aphorisms of his great preceptor, Boerhaave. For him the fons et origo mali in gout was disturbance of the functions of the alimentary tract.