The constitutional disturbance is often profound, certainly out of all proportion to the severity and extent of the local phenomena. Especially prominent are the nervous concomitants—the excruciating pain, the irascibility, etc. Viewing these in light of the paroxysmal nature and periodicity of gout, Duckworth postulated a kinship between the disorder and the paroxysmal neuroses. But, given an infective element, what more plausible than to attribute the nervous phenomena of gout to the simultaneous action of its toxins on the higher centres?
The temperature curve, again, is obviously compatible with this conception. It begins abruptly, its course punctuated by daily remissions. No specific peculiarities apparently differentiate it from other arthritides of established or assumed infective origin, but its relatively low grade pyrexia recalls that typical of gonococcal arthritis. Its most striking feature, however, is the disproportion between the level of the pyrexia and the intensity of the general and local phenomena. Moreover, the temperature is not only low, but relatively ephemeral in duration, while the inflammatory reaction in its violence emulates that of the most sthenic forms of arthritis.
Albeit both the febrile disturbance and the local reaction display infinite grades of severity. Thus, acute gouty polyarthritis may be afebrile and the asthenic varieties of the affection marked by little inflammatory reaction. All these vagaries, however, are quite compatible with infection—the reflex, as it were, of varying degrees of toxæmia.
Says Duckworth, “The pyrexia proper to acute gout is paroxysmal with remission, and the pain of gout is likewise paroxysmal. One is reminded of the influence of marsh poison upon the nervous centres. This paroxysmal no less than periodic element in gout stamps a nervous character upon the malady and binds it in alliance with other well-recognised neuroses.”
How interesting these reflections by this distinguished physician in light of latter-day revelations! For, in so far as these features in gout are reminiscent of malaria, they disclose an affinity, not for a malady of nervous, but one of established infective, origin.
Simultaneously with the onset of pyrexia the pulse quickens. The blood shows that increase in fibrin characteristic of inflammation, a fact noted by Gulland, Cabot, Buchanan and others. But more significant is the presence of leucocytosis. It may be of high grade. In a case of acute gouty polyarthritis recently under my care the leucocyte count reached 27,000. Even in a subacute example of the classic monarticular type the leucocyte count attained 25,920. It was of leucoid type and attended by moderate anæmia due to deficiency of red corpuscles.
Nor is leucocytosis restricted to the periods of exacerbation, but it may be met with in the inter-paroxysmal stages. In my experience, even in cases of definitely chronic type it may reach 14,000. The higher grades of leucocytosis are obviously very suggestive of an infection, and that lesser degrees should be encountered in examples of definitely chronic type seems to point to gout being of the nature of a chronic or serial infection.
I would here add also that the converse of leucocytosis, viz., leucopenia, is sometimes met with in chronic cases. Dr. Munro and I have met with two instances of such in chronic gout in the intervals between paroxysms. This decrease in the number of leucocytes (leucopenia) is, of course, deeply interesting and, needless to say, quite compatible with infections, e.g., enteric, malaria, tuberculosis. In fact, it suggests that gout may be the outcome of divers infections, and not due to any specific organism.
Enlargement of the lymphatic glands was, by older authors, believed not to occur in gout. But obviously the lack of macroscopic evidence does not exclude the possibility of microscopic changes in these structures. The likelihood of such, moreover, is enhanced by the occasional occurrence of lymphangitis in connection with the inflammatory articular lesions. Buzzard, indeed, long since claimed that there was “clinical evidence of subacute gouty inflammation of lymph spaces in certain regions due to uratic deposit and influence.”
As a matter of fact, enlargement of the lymphatic glands does occur. Thus, my colleague James Lindsay cites an instance thereof. The subject, a painter, fifty-three years of age, had gout of some three years’ standing. During an acute paroxysm thereof “there was a mass of glands in the right groin, synchronous with an acute inflammation affecting the right knee and periarticular tissues. On the subsidence of the gouty inflammation the glands became smaller, but never entirely disappeared during the four weeks he was subsequently under observation.”