Gout, with a section on ocular disease in the gouty

by Llewellyn J. Llewellyn

The Evolution and Life History of Gout

If the onset, phenomena, and course of acute gout are reminiscent of infection, so, also, does a review of the life history of the disease, as a whole, carry with it the same inference.

For the course of gout, like other arthritides of chronic type, is not one of steady, uninterrupted progress, but one marked rather by periodic or intermittent advances, as if seemingly due to a series of successive infections or sub-infections. One is reminded of gonococcal arthritis in its more severe forms, the acute exacerbations which chequer its course being generally referred to intermittent absorption of fresh doses of the toxin from some smouldering infection in the prostatic urethra.

Now, if the general course or evolution of gouty arthritis is notably similar to that of the specific infective arthritides, so, also, do the clinical features approximate. Thus its onset, more often than not, is abrupt and attended by pyrexia of irregular or septic type, with an occasional leucocytosis.

Again, that not all cases of gout are of acute fulminant type may be admitted. We know that it may assume the guise of a fleeting arthralgia or “flying gout,” a transient synovitis, as well as an acute arthritis of mono-, oligo-, or poly-articular extent. This same polymorphism in respect of the joint lesions in gout is a replica of that met with in the specific infective arthritides. The milder varieties betokened by arthralgia or synovitis tend commonly to disappear, as it were, spontaneously in precisely the same manner as the arthralgias or synovites that follow the exanthemata, and we presume that, comparably with these latter, the source of infection dries up and restitutio ad integrum of more or less completeness follows.

But with repeated attacks, as in the specific infective arthritides, progressive infiltration and thickening of ligaments, capsule, and related tendinous and aponeurotic structures ensue. As far as these anatomical changes are concerned, gouty arthritis and the specific arthritides are at one, but with this outstanding difference, the associated uratic deposition. Save in respect of this last, the analogy is complete, and herein resides the specificity of gouty arthritis.

Chalmers Watson, from his observations of “gouty deposits” in human subjects in their relation to tendons, cartilage, and bone, came to the conclusion that the tout ensemble of the pathological lesions was very reminiscent of that typical of the more chronic types of infective disorders. Thus necrotic areas in gouty tendons stood in such clear relationship to the vascular supply as to suggest some infection viâ the blood-stream. Again, areas of erosion in the cartilage were found to be due, not to uric acid, but to the disintegrating action of small round cells of the nature of granulation tissue.

As to uratic deposits located in the bones, it was noted that their vicinity was characterised by marked vascularity, the existence of giant cells, and an accumulation of the small round cells so commonly correlated with the action of bacterial toxins.

In reviewing the foregoing clinical and pathological data and, alike, the inferences as to their significance, it cannot, we think, be gainsaid that, collectively, they are more readily explicable as being due to an infection than to any other morbid source.