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. MORBID ANATOMY It has been truthfully affirmed that we know more of the _results_ or products of gout, and less of its _essential_ nature, than of almost any other disease. Thus the post-mortem history of the disorder is concerned almost exclusively with more or less graphic accounts of the _uratic deposits_, their sites of predilection, and the changes that they induce. Hence it is that the morbid anatomy of gout relates for the most part to its _regular_ or _articular_ manifestations, for it is in and around the joint structures that the deposits for the main part occur. As to the assumed localisations of the disease in the _internal_ organs, there is no _anatomical_ evidence that they are due to an invasion of the “gouty” inflammation. Not even the _renal_ changes, despite the attestation, as it were, of the gouty process by _uratic deposits_ in the _papillæ_, can be held as distinctive of gout. Norman Moore found them present in only twelve out of eighty cases. As Osler said, “The presence of uratic concretions at the apices of the pyramids is not a positive indication of gout. They are not infrequent in this country [U.S.], in which gout is rare.... It is not possible to say in a given case that the condition has been due to gout unless marked evidence of the disease co-exists.” If, then, nothing distinctive can be claimed of the _renal_, how much less can we construe as “gouty” the anatomical alterations that may or may not be met with in other organs in this disorder. In short, it may be said of the _renal_ as well as the other _visceral_ lesions, so often met with in association with gout, that they are met with even more frequently in its absence, and most certainly fail to attest their “gouty” nature by the appearances which they present.