_Inflammatory reaction_ is, we hold, an invariable _antecedent_ in all gouty processes, whether of _articular_ or _ab-articular_ site. Granted that inflammatory reaction is a necessary prelude, the specificity of gout is attested by the fact that this same is followed by the deposition of urates. But while the sequential uratic deposition invests all forms of “gouty” inflammation with a specific character, unshared by any other disease, it follows that the cause of the said inflammation must, if possible, be ascertained. For Walker Hall “the contention that gout lowers the general tissue resistance, and so opens the way to bacterial infections, is so obvious that it need hardly be formulated.” In light of this, we need have the less diffidence in hazarding our opinion that the morbific agent responsible for “gouty” inflammation is an _infection_ or _sub-infection_. Now, in all forms of arthritis other than gouty, the intrusion of a germ is held to be self-explanatory and final; in short, all the local morbid changes and constitutional disturbances are held satisfactorily accounted for by the organism or its toxins. The problem of gout, however, is not so simple. Its arthritis is peculiar in that it is always accompanied or followed by _uratic deposition_, which, be it noted, is not an ordinary sequel of inflammation. It is, in short, the outcome of inflammation supervening in an individual of _gouty diathesis_. What do we know of this latter? The researches of the bio-chemists reveal that _uric acid_ is the end-product of nuclein metabolism—the summation of a long chain of enzymatic reactions. Some indeed have thought to find an adequate explanation of gout in _enzymatic abnormalities_. Thus, Adami and McCrae suggest that gout is the outcome of _insufficient oxidation_, whereby the precursors of uric acid and similar bodies are not fully oxidised, and, by their accumulation and toxicity, set up morbid changes, and the uric acid formed is, in its turn, imperfectly oxidised and accumulates. This diminished oxidation is due to a constitutional deficiency of _oxydases_, inherited or acquired. This opens up the old problem as to whether uric acid is an intermediary or a terminal product of metabolism. But, from evidence cited in preceding chapters, it appears probable, if not certain, that uric acid is an end-product. Moreover, as Gideon Wells observes, “the failure of recent studies on the enzymatic transformation of purins to locate anywhere in the human body an enzyme-destroying uric acid makes hazardous the attempt to explain gouty metabolism as a result of enzymatic abnormalities.”