Summary
In conclusion, we have now dealt with those factors currently regarded as predisposing causes of gout. Personally, as I have before said, the differentiation of the foregoing from the so-called exciting causes of gout is purely arbitrary. Thus even those who countenance such division are forced to admit that many of the predisposing causes will, “if at any time suddenly increased,” immediately excite a fit of gout.
In other words, the difference is quantitative rather than qualitative. Thus, a moderate drinker, if perchance he exceed his usual limits, pays the penalty by an outbreak. Another habitually addicted to the fleshpots eclipses himself, and a similar retribution is exacted. Or, he exposes himself to a chill, with subsequent gastro-intestinal or hepatic functional derangement. Yet again, the cessation of wonted exercise, and more often the taking of it when unaccustomed, may determine the onset of a paroxysm.
But far more arresting are the numerous and well authenticated instances in which local trauma not only determines an outbreak but also its locality. How frequently, too, have blows, strains, sprains, fractures, dislocations, or other trivial or severe injuries, been the signal for an attack. Now, as we hope to show later, local foci of infection are extremely common in the gouty. Such are especially frequent in the teeth, tonsils, naso-pharynx, etc. Is it not then extremely probable that organisms may, viâ the blood-stream, find their way to a joint, the resistance of whose tissues has been lowered by a trauma, however slight its degree? This I apprehend to be the true explanation of the undoubted intimate connection between traumatisms and arthritic outbreaks of gout.
Of similar significance, too, the numerous instances on record in which acute attacks of gout have followed acute tonsillitis, acute pharyngitis, acute parotitis, etc. How frequently, also, competent observers, such as Garrod, noted that boils and carbuncles frequently appeared to be excitant of acute attacks. But to this important point, the intrusion of an infective element in the genesis of gout, we shall return in a later chapter entitled “Gout as an Infection.” It will suffice here if we record our belief that—
(1) Heredity is the sole predisposing factor in gout.
(2) That the differentiation between the usually cited predisposing and exciting causes is unwarrantable.
(3) That both alike are merely determinants.
(4) That their influence as such in exciting outbreaks is exerted through the medium of infection, this achieved either directly or indirectly.