Clinically it manifested itself by a variety of symptoms—depression of spirits, irritability, lethargy, headache, pains and aches in the limbs, vertigo, insomnia, dyspepsia, palpitation, raised blood pressure. Such were the motley group of disorders affiliated by Murchison to lithæmia. But his disciples, more ardent, set no limit to the manifestations of uric-acidæmia.
Not only gout, but rheumatism and allied disorders, were amongst its progeny, and Osler tells us that one writer enumerates not fewer than thirty-nine separate morbid conditions associated with lithæmia. But leaving aside the extravagant claims of Haig and his followers, the impression even now is but too prevalent that gout and lithæmia are convertible terms. There is little or nothing to justify the assumption that an increased output of uric acid in the urine or deposition of urates therein is diagnostic of gout. Such, moreover, presupposes the further assumption that uric acid is the cause of gout.
We may affirm that certain symptoms betoken malassimilation of food or defective tissue metabolism. But it is by no means certain, as Murchison held, that a functional disorder of the liver is the fons et origo mali, much less that uric acid is the sole noxious substance. Yet in a masterly discussion of the subject Pratt, of Boston, tells us that as recently as 1895 a “leading clinical teacher” affirmed that “headache, migraine, depression of spirits, shooting pains, cramps, palpitation, vertigo, are a part of the symptomatology of lithæmia.”
Surely, if we are to make any pretence of reducing the phenomena of lithæmia or irregular gout to a scientific precision worthy of the present status of medicine, we should fight shy of such sweeping assertions. The caveat, we fear, is not superfluous. For as that judicial physician, Austin Flint, once satirically observed, “the designation ‘uric acid diathesis’ is used by some physicians in a rather indefinite way to describe various morbid states which may not at any time be accompanied by deposits of urates, and in which there is no proof of an excess of uric acid in the blood.”
Caustic as was this stricture, it was no less prophetic than apposite. For recent blood analyses have, as Pratt states, demonstrated that there is no increase of uric acid in the blood in that medley of disorders attributed by Murchison and his followers to “lithæmia,” or “the uric acid diathesis.” Here we would inveigh strongly against the too prevalent habit of stigmatising as “gouty” such symptoms as headache, vertigo, palpitation, etc., not only without any evidence of their being of this nature, but frequently when no attempt has been made to eliminate “errors of refraction,” aural disorder, etc. Moreover, granted that such possible sources have been excluded, we have no justification in invoking “gout.” For, as noted, all modern observations fail to demonstrate the presence of uricæmia. Under such circumstances, given that the anomalous symptoms are inexplicable, would it not be wiser to content ourselves with the assumption that their presence postulates, not lithæmia, but a toxic condition of the blood plasma? This at least carries with it the inference that a search should be made for the focus of toxic absorption, whereas for but too many the term lithæmia, even when undemonstrated, is held to be self-explanatory and final.
Turning to another aspect of this subject, we are reminded by Duckworth that Hutchinson “directed attention to various maladies affiliated with what he terms rheumatic gout and gout, but differing somewhat from both, and these include various eye troubles, such as iritis, hæmorrhagic retinitis, and some forms of glaucoma, lumbago, sciatica, chronic rheumatoid arthritis, Heberden’s nodes, and possibly hæmophilia.”
As to the so-called “gouty” origin of the various eye troubles, these will be dealt with separately by Mr. Beaumont in his section. For the rest, hæmophilia may, we think, be safely discarded, Heberden’s nodes relegated to osteoarthritis, while rheumatoid arthritis has long since vindicated its claim to clinical individuality.
But as to lumbago and sciatica, these cannot be so easily disposed of, as a reflection of Heberden’s brings home to us. “It must be owned,” says he, “that there are cases in which the criteria of both are so blended together that it is not easy to determine whether the pain be gout or rheumatism.” Our own attitude towards this vexed point was precisely defined in a previous chapter in which we dealt with the affinities between gout and other diseases.
Having dealt with the broader and more extravagant claims made on behalf of the clinical content of irregular gout, we now restrict our purview to those disorders, chiefly visceral in site, which even to-day are referred by some to this category. We shall in the first instance deal with that variety known as retrocedent gout, and shall subsequently proceed to discuss other so-called irregular manifestations of the disorder.