This last is, I think, apt to be forgotten, and gout vicariously saddled with all the infirmities of age. Thus, out of 2,680 examples of arterio-sclerosis Huchard held gout and lithiasis responsible for no less than 693. An appalling indictment, but what of the long arm of coincidence? For age unquestionably is the chief factor in the production of arterio-sclerosis, though many allot gout a dominant rôle in its genesis. This certainly is by no means proven. Still, whatever be the relationship, gout and arterio-sclerosis are very often found in association. If so, the prognosis will obviously rest, not on the gout, but on the vascular disease—the pulse tension. If therewith be correlated albuminuria and a displaced apex beat, the outlook is unfavourable.
Again, is the subject lean or obese? If the former, so much the better, for corpulency and gout are a sinister combination. Gout in itself, as previously observed, favours microbic invasion, and obesity accentuates the liability. Moreover, the gouty obese are prone to arterio-sclerosis and granular kidneys, with sometimes a superadded glycosuria, or even true diabetes. In such subjects also the presence or absence of signs of cardiac mural degeneration must enter into our forecast, which at best is but gloomy.
Apart from arterial degeneration, we have to recollect the tendency to phlebitis of recurrent type. This when present always carries with it the risk of embolism and sudden death. Cases therefore displaying this proclivity to phlebitis must be judged accordingly. The gouty glycosuric, too, is always subject to the risk that the condition may develop into one of true diabetes. The absence of response to dietetic restrictions, viz., persistent sugar in the urine, the onset of thirst, polyuria, or other concomitants of diabetes, will darken the prognosis.
Also I myself believe that the presence of local foci of infection gravely prejudices the course of gout, accentuates any tendency to recurrence of the attacks, and incidentally reinforces any latent proclivity to vascular and visceral degenerations.
Last, but not least, what of the subject’s habits? The “internal environment” of the tissue cells of the gouty is presumably of itself none too good; but if to this be added the poison of alcohol, lead, or the toxic products of gluttony, it is incalculably worse. The painter or the plumber, if he can, would be wise to change his calling. If the alcoholic be deaf to remonstrance or the glutton continue to gorge, their chances of life dwindle proportionately, and if given to both vices, still more so.
In conclusion, the prospects of long life in gout depend in the main on the presence or absence of associated morbid states. If there be no complications such as I have indicated, the disease, in my experience, is not likely to shorten life materially, always provided that the victim is amenable to what should be the watchword of the gouty,—
“The rule of not too much, by temperance taught
In what thou eat’st and drink’st, seeking from thence
Due nourishment, not gluttonous delight.”
Milton.