(1) Slight fluctuation in the endogenous excretion.
(2) Low endogenous average.
(3) Small percentage of exogenous purin nitrogen excreted as uric acid nitrogen.
To sum up, then, we see that poisons, other than those responsible for gout, may engender obliquities of general metabolism, with disturbances of purin assimilation and output, viz., lead, alcohol, and the causa causans of rheumatoid arthritis. Also, in respect of lead poisoning and alcoholism, further affinities with gout are discernible in that, like the latter disorder, they tend in their later stages to be associated with arterio-sclerosis and renal inadequacy.
Infantile Gout
Apart from the fact that gouty arthritis may occur in young children, Comby and other observers have noted that children born of gouty parents display a tendency to inflammatory changes in the cutaneous tissues and also in the mucous membranes.
These proclivities are difficult of explanation, but some further observations by Czerny, Paltauf, Escherich, and Pfaunder are also worthy of note. Under the headings of “exudative diathesis” or “neuro-lymphatismus” they have described a symptom complex marked by lymphatism with asthma, occasional vomiting, defective nervous equilibrium, and eosinophilia. These varied phenomena also are common in the descendants of gouty, diabetic, and arthritic subjects.
The clue to the true nature of these phenomena may possibly reside in the fact noted and emphasised by Uffenheimer, viz., that these children exhibit a purin metabolism identical with that met with in gouty patients.
From the foregoing consideration it is clear that further observations are called for in the sphere of purin metabolism, and it is, perhaps, not too much to hope that extended investigations of the uric acid content of the blood may clarify and illumine the conflicting results obtained by urine analysis.
As before stated, we had intended in the next chapter dealing with the question of “Uricæmia in Gout,” but on second thoughts it appears desirable to us to interpolate a chapter devoted to discussion of the primary renal origin of gout; for we take it that, with the phenomena of uric acid excretion in gout fresh in our minds, it will be more easy at this juncture to attempt solution of this very intricate problem. This achieved, we shall resume our thread and pass to the consideration of uricæmia and subsequently uratosis in gout.