“It is not a sacred disease. There will therefore be no profaneness in handling it freely,” affirmed Benjamin Rush of gout some hundred years since.

Nevertheless one approaches with diffidence this debatable ground, so hedged in by high sanction and tradition. Albeit reverence for authority must, in the interests of progress, be tempered by that spirit of inquiring scepticism which would sift the chaff from the grain, this the more emphatically in that of all morbid conditions “irregular” gout, by the very vagueness of its clinical content, lends itself the more easily to unbridled inference, hazardous conjecture, and fanciful surmise.

As for the unlicensed freedom too often exercised in relegating disorders to this category, Rush would appear to have out-heroded Herod, pace the following rhetorical reflections, for they could scarcely rank as clinical observations. “The great toe and the joints of the hands and feet are no more its exclusive seats,” said Rush, “than the stomach is the throne of yellow fever. In short, gout may be compared to a monarch whose empire is unlimited. The whole body crouches before it.... The gout affects the glands and lymphatics. It produced a salivation of a profuse nature in Major Pearce Buller, which continued for two days. It produced a bubo in the groin in a citizen of Philadelphia. He had never been infected with the venereal disease. Of course no suspicion was entertained by me of its being derived from that cause.... Scrofula and all the forms of dropsy are the effects in many cases of a disposition of the gout to attack the lymphatic system.... A distressing collection of air in the rectum, which renders frequent retirement from company necessary to discharge it, is likewise a symptom of gout.”

It is difficult to conceive that any such pronouncement could have emanated from a physician of Rush’s standing and repute, a contemporary, be it noted, of Heberden, to whose masterly commentaries on the history and cure of gout all posterity is indebted. Nevertheless as recently as 1854 Sir Spencer Wells claimed that “any attempt to describe the nervous diseases of females caused by gout would lead to an enumeration of almost all forms of their diseases, especially those usually considered as hysteric. The intestinal derangements with tympanitis, neuralgia, or colic, the hysteric pain in the right epigastrium, the cardialgia and gastrodynia, the hysteric vomiting and epigastric spasms, the morbid sensibility of the pharynx and fauces, hysterical palpitation, asthma or bronchitis, loss or alteration of the voice, some forms of hysteric paraplegia or hemiplegia more or less complete, chorea or tetanus, some of the curious paroxysmal affections observed in hysteria, and all the varieties of neuralgia and simulated inflammation, commonly called hysteric, frequently arise from the presence in the blood of the impurities which are the true characteristics of gout.”[43]

Truly, in light of this heavy indictment, one scarcely wonders that Rush classed the domain of gout as limitless. But one must recollect that, nosologically speaking, our forefathers were sadly hampered. Anomalous symptoms and disorders had to be referred to one or other of the available titles of disease, and what term more elastic than the timeworn “gout,” so easy to saddle with vicarious responsibilities?

But pari passu with advancing knowledge of the pathology of the nervous system and the rise of hysteria to the status of a clinical entity gout was shorn of the excrescences heaped on it by Laycock, Wells, and others.

But nevertheless the emancipation of gout from nervous and other alien disorders was slow of achievement, and largely, I think, through the wide acceptation of Murchison’s theory of a pathological state allied to gout and termed by him “lithæmia,” or the “uric acid diathesis.”

According to this authority, the deposit of lithates in the urine is a “manifestation of a morbid condition of the blood and of the entire system,” the outcome of a functional derangement of the liver. Such hepatic disturbance might endure for years without manifesting any other symptom than a frequent deposition of urates and occasionally uric acid in the urine. But, added Murchison, the same if neglected “may ultimately be the means of developing gout.”

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.

Retrocedent Gout

The term retrocedent or suppressed gout still lingers in medical nomenclature, largely, we think, as a tribute to tradition, for rarely indeed is it invoked in current literature. Known since the days of Galen and Aretæus, it originally signified a condition in which sudden inhibition of the acute joint affection is followed by or coincides with the development of serious internal symptoms referable either to the gastro-intestinal, cardio-vascular, or nervous system. Thus, there may be, e.g., vomiting, diarrhœa, dyspnœa, cardiac arrhythmia, cerebral hæmorrhage, delirium or coma.

Naturally for our forefathers the abrupt subsidence of the joint disorder with the incidence, as fulminant, of severe and alarming visceral symptoms appeared to be an example of true metastasis. That death, tragically sudden, so often ensued, but rendered more imperious the necessity for explanation; and, in the then state of knowledge, the proffered assumption could hardly be regarded as anything other than a perfectly legitimate and useful hypothesis.

The retrocession of the articular affection in acute examples of gout ensues abruptly, but in chronic types it usually transpires more gradually. Often no cause is assignable, but frequently the so-called metastasis has followed exposure, chill, or the imprudent application of cold to the inflamed joints. The late Dr. Parry, of Bath, in one winter saw two instances of apoplexy follow “the removing of gout in the extremities by immersing the feet affected in cold water.” In some, following the same revulsive procedures, severe cardiac pain has ensued with syncopal attacks, sometimes fatal, while in others gastro-enteric symptoms of like gravity have developed.

It is the asthenic types of gout that, according to Duckworth, are most prone to metastasis. When the phenomena occur rapidly, flitting from place to place, they have been designated “flying gout.” Nevertheless, as before said, the most dramatic examples arise in acute sthenic gout, though in their instance less likely to occur spontaneously than in sequence to depressing external agents, e.g., cold lotions, etc.

Reviewing the recorded examples of retrocedent gout in the light of latter day experience, it is, we think, most significant that no such dramatic examples apparently occur nowadays, at least none to which the term “retrocedent gout” appears applicable. The designation, indeed, bids fair to become obsolete. What then is the explanation? That even to-day cases of acute articular gout yield to, or are replaced by, functional visceral disturbances, of varying degrees of gravity, is certainly true. But, partly through increase of knowledge and partly through the growth of a more critical attitude, we seldom, if ever, feel justified in ascribing them to gouty metastasis.

Take “gout in the stomach,” to which organ, in the days of the Regency, it appeared to fly on the slightest pretext, a “vulgar belly-ache taking rank by courtesy” as such, before Sir Thomas Watson pricked the bubble of these pretentious ailments by his suggestion that “gout” (so called) in the stomach sometimes turned out, under the test of an emetic, to be nothing more than pork in the stomach. A caustic stricture, but doubtless well merited. For the symptoms held typical of “gout in the stomach” are but those of gastric irritation, with nothing to suggest that they are of “gouty” origin.

Again, as Brinton in his classic exposure of this clinical myth observes, some of the recorded instances doubtless derive their melodramatic aspects from unrecognised biliary colic. As he rightly says, some of the cases instanced by Scudamore were jaundiced usque ad unguem. Gallstones, too, are among the many derivatives of the so-called “gouty” habit. The age incidence of both disorders is identical, whence doubtless the conception of the relationship. But what of the abdominal catastrophes attached to gallstones, all wholly unguessed at in those days? What, too, of the unrecognised and doubtless frequently coincident renal disease, with its menace of uræmia—pain, vomiting and prostration, not to mention Buzzard’s reflection that some cases of gout in the stomach were probably referable to gastric “crises,” i.e., tabes dorsalis?

If we recall that none of these sources of fallacy—and we have named but the more common—were eliminated, and also the absence of any anatomical proof post mortem of gastric lesions, one may well ask with Brinton, “Is there any ‘gout in the stomach’ left after the subtraction of these various affections?” Personally, I can say with Brinton that “I know of no such case; have never seen one; have never been able to get trustworthy evidence of one from some of the most accomplished physicians living, or from the best records.”

Reverting to the cardiac and cerebral phenomena that have sometimes followed the retrocession of acute gout, the same difficulties confront us. The conclusion that they are examples of retrocedent gout is drawn from premises which really do not support it. Strictly speaking, there is nought but the time relation to go upon, and the laconic comment “Non sequitur” is obvious.

To continue, the more we know of the causes and effects of disease, the less relevant becomes the time relation, and the nearer do our conceptions of cause and effect approximate to the more truly valid conception of ground and consequence. But what grounds have we for assuming that the anginal, the syncopal attack, or the apoplexy is the consequence of gout, that it is exclusively due to the materies morbi of gout?

The very disparity between the local lesions seems to exclude the possibility of their being due to one and the same cause: in the joint, acute inflammation; in the heart and brain, degenerative changes. Where then the nexus? Surely it is but a time relation, a coincidence, the outcome of, concurrent though unrelated cardiac and vascular lesions. In short, the cases of so-called retrocedent “cardiac” and “cerebral” gout usually resolve themselves into cardio-mural degeneration, arterio-sclerosis, or renal disease.

Other Irregular Manifestations

The more dramatic examples of retrocedent gout, as before stated, occur mainly in the acute varieties of the disorder. But the same visceral metastases are occasionally linked up with the less severe articular manifestations, or with that vague clinical entity known as “goutiness,” the same being frequently known as “wandering” or “flying” gout. Most of the examples met with in the present day belong to the last category. This may possibly find its explanation in the growing infrequency of the more acute or sthenic types of gout.

Both of the mild and of the severe forms of metastasis the same pathological interpretation is hazarded. The gout is described as “suppressed” or “retrocedent.” According to the former conception, the gouty process itself suffers inhibition, while the latter term signifies deflection of the materia peccans of gout from the joint into the viscera. Of the twain the former hypothesis seems to me the more plausible. Thus, given an acute gout at its inflammatory zenith, it is conceivable that, if abruptly checked, the same might reflexly precipitate the occurrence of internal lesions in structures undermined by insidious and pre-existing degenerative changes. In other words, the aborted attack is not the cause, but the occasion, of the cardiac failure, the apoplectic stroke, the uræmia, etc.

On the other hand, given that such were due to actual transference of the gouty poison, one would expect that it would induce the same inflammatory phenomena in the viscera as in the joint. But there is no anatomical proof that such occurs, no evidence of an actual invasion of the impeached viscus by the gouty inflammation. Uratic deposits have, it is true, been found post mortem at the site of visceral lesions, but, be it noted, generally in degenerating tissue altered by other morbid processes. Some, however, affirm that in such the gouty process has quâ the uratic deposits left, so to speak, its attestation behind it.

But any degenerative focus may in a gouty subject become the seat of such a deposition. Yet it would be presumptuous to infer its gouty origin from this fact alone. Such are common in chronic nephritis, and this apart from gout. What need for wonder then that the same should occur in gouty subjects, with their blood surcharged with uric acid?

Were such uratic deposits located at the site of inflammatory as opposed to degenerative visceral foci, it would to our mind give more colour to the assumption that they were the outcome of a true gouty process; in other words, that, as in the joints, they were the sequel or concomitant of acute gouty inflammation. But it is not so.

As for the structural or organic degenerations met with in gouty subjects, very many, if not all, as Longstreth rightly says, “belong to some one of the great general classes of tissue changes, some of which are due to special causes, but the most of them own many causes. One of these many causes can be under certain circumstances gout, but there is really nothing special in the appearances by which we can unequivocally pronounce them of gouty origin.” With this view few would join issue, save only the reservation that the scleroses so commonly met with in gout, if due thereto, must owe their origin to some more vital agent than uric acid, a few milligrammes more or less in the blood content thereof.

It will be seen then that the anatomical evidence that gout can affect the internal organs is wholly lacking. The criteria then upon which the assumption is based that this or that functional disturbance is a manifestation of irregular or visceral gout are wholly clinical.

Doubtless the conception of irregular gout was derived from “the unaided operation of custom.” Thus, when one clinical event, A, was noticed frequently to precede another, B, the idea of an association between A and B was generated, and by virtue of this association A was said to be the cause of B. But obviously the fact that B has followed A does not establish any necessary connection between the two clinical events. In other words, the idea of a causal relation is in a sense a purely intellectual feat, a clinical inference presumptive and retrospective.

The evidence that a relationship exists between irregular and regular manifestations of gout rests upon the following sequences and alternations of clinical events:—

As before noted, digestive troubles frequently precede the initial outbreak of articular gout. The same likewise are frequent in chronic cases between the intervals of arthritic seizures.

Now it has been customary to regard the alimentary or other disturbances that precede an initial articular attack as “gouty,” and likewise those that intervene between the gouty paroxysms in long-standing cases. In other words, in light of the subsequent articular outburst, what was mysterious ceases to be a mystery. All the vague “acidities, flatulencies, megrims, and biliousnesses, of whatever occult kind,” are forthwith hailed as “gouty,” this merely upon the ground of the sequence of clinical events, because the symptoms have disappeared from, e.g., the stomach to reveal themselves in the joint or joints, or vice versâ.

Now my own view is that the antecedent hepatic or digestive disturbances that so frequently precede initial attacks of gout are in all probability, nay assuredly, not gout. They should rather be regarded as the cause, the foundation, of the malady than its effect, a cause inoperative save in the presence of individuals victimised by inherent morbid tissue potentialities. For similar symptoms are but too common in the non-gouty. They are very common antecedents of, e.g., rheumatoid or atrophic arthritis. Nevertheless we do not when the arthritic disorder subsequently manifests itself talk of the preceding digestive disturbances as “rheumatoid” dyspepsia. Then why this presumptive and retrospective diagnosis of similar prodromal phenomena as “gouty” dyspepsia? For there is pending the articular outbreak nothing distinctive in the digestive derangements, nothing that would enable us to diagnose them as “gouty.” They might, for aught we know, be significant of oncoming rheumatoid arthritis.

Now in the case of the latter we regard the prodromal digestive phenomena as probably indicative of some infection located somewhere in the alimentary tract. It would be wiser, I think, to adopt the same attitude in regard to our “gouty” examples. Moreover, as we know, such dyspeptic symptoms recur from time to time throughout the life history of both rheumatoid and gouty arthritis. In the former disorder we regard them as indicative of recurring infection, followed as they so uniformly are by exacerbations of the joint trouble. Is it not time we adopted the same attitude towards the gastric or hepatic functional disorders that punctuate the course of chronic gout with a periodicity that rivals that of the articular paroxysms?

Unquestionably to my mind when we have regard to the extreme frequency with which local foci of infection, e.g., oral sepsis, etc., are found in gouty subjects, this would be the more rational attitude, the one more in conformity with modern medical thought.

But if we would condemn those who, in the presence of unequivocal tokens of gout, label antecedent or intercurrent dyspepsias, etc., as “gouty,” what are we to say of those that even in patients who have never had regular gout or exhibited tophi yet presume to classify their associated digestive troubles as “gouty”? This, I contend, is wholly unjustifiable. I would say more, that such conjectures are hazardous in the extreme, this both in the overtly gouty as well as in the non-gouty. I recall the instance of an individual who suffered from classical articular gout which palpably alternated with attacks of abdominal pain, but the clue to the true nature of the latter symptoms, as revealed at operation, was a chronically inflamed appendix. If so in this case, how many so-called “gouty” acidities have resolved themselves into appendicular or gall-bladder dyspepsia!

My conclusion then is that the gastro-intestinal disorders attributed to gout cannot legitimately be regarded as examples of irregular gout. They should not be held “symptomatic” of, but etiologically related to, gout, a view more calculated to lead to exact diagnosis and rational therapy, and incidentally to elucidate the true nature of gout.

In respect of other organs and the symptoms connected with them in “gouty” persons the case is very much the same. Always and ever are we confronted with the same difficulty, inability to determine whether antecedent, co-existing, or consecutive affections in certain examples of gout, are not associated merely by coincidence.

Disturbed cardiac action is not uncommon in gouty subjects, palpitation and arrhythmia and syncopal threatenings, and frequently symptoms difficult of differentiation from true angina pectoris.

I am reminded of an old physician whom I saw in consultation some years ago, who suffered from alarming attacks of precordial anxiety. He was well on in the sixties, and very obese. He was convinced that his cardiac irregularities, etc., were of gouty origin, and often exclaimed regretfully: “If I only dared to take two bottles of port, and got it in my toe, all would be well.” He had never had an articular outbreak, and based the diagnosis of his case on the fact that from time to time his urine for long since contained excess of urates. Having suffered much of many physicians, he at last grew restive, took the bit between his teeth, rushed to a spa, and forthwith embarked on a very strenuous course of “waters and baths.” At once he got a severe attack of acute polyarthritic gout, and mirabile dictu, all his cardiac troubles straightway ceased.

Retrospectively viewed, many would regard the preceding cardiac condition as of “gouty” source. That the old gentleman, of florid countenance, plethoric build, and lethargic habit, was potentially “gouty,” there is no doubt. But he was also abnormally fond, not of alcohol, but, curiously enough, of sweetmeats and cakes of all sorts, hence “dyspeptic.” He had a feebly acting heart, but no detectable valvular lesion, though mural degeneration seemed likely. My own diagnosis was flatulent dyspepsia with secondary cardiac disturbance, and finally acute gout, the exciting cause of which, as I have so frequently seen, was a course of hydrotherapy. The patient never regretted his venture, and, I am glad to say, lived for some years.

Such cardiac paroxysms are not uncommon in the “gouty,” and, alarming though they are, I question if purely functional disturbances of this nature ever prove fatal. As to the valvular lesions and mural degenerations observed in the “gouty,” there is little or no evidence that they are dependent on gout. Indeed, the lack of a tendency to endocarditis is one of the criteria distinguishing gout from acute rheumatism. I note that in one textbook pericarditis is classed among the cardiac manifestations of irregular gout. But it must not be forgotten that renal disease, a frequent concomitant of gout, predisposes to pericarditis, which, indeed, occurs in granular kidney even when unassociated with gout.

As to the respiratory organs, such chronic maladies as bronchitis and asthma are very frequent in the “gouty,” but I question if they are more so than in non-gouty subjects. In any case their symptomatology and course are the same whether gout be present or not. Much, too, has been made of the fact that asthmatic and arthritic manifestations may alternate. But we must recollect that asthma per se has a paroxysmal tendency; it has a tendency to periodicity and a liability to be excited or aggravated by much the same factors as favour outbreaks of gout. It is said, too, that there is a “gouty” pneumonia, and that the same has been replaced by an acute articular paroxysm. But, in respect of all these alleged “gouty” respiratory disorders, would it not be more scientific to cease talking of them as “gouty” and instead to speak of them as bronchitis and asthma occurring in “gouty” subjects? This, I may remark, is not to say that we should take no count of the reigning diathesis in our treatment of all associated affections.

Of the nervous phenomena relegated to gout we hear nowadays less and less. “Gouty” headaches are almost a thing of the past. The acute “gouty” delirium of older writers in many cases was but an euphemism for alcoholism, and likewise the spinal paralyses; while the convulsions and comas were certainly almost always attributable to uræmia. It would be held rash to-day to speak, like our forefathers, of “gouty” cystitis, urethritis, or orchitis, for there is no evidence of any pathological connection between them; and the same stricture is also applicable to the many cutaneous affections affiliated without sound pretext to the materies morbi of gout.

In the early part of the nineteenth century the French school were most insistent on the prevalence and variety of the cutaneous manifestations of l’arthritisme; but even by them the all-pervading influence of gout in the etiology of skin disorders is no longer held even as a working hypothesis.

Conclusions.—The sum of my experience and reflections on so-called “irregular” gout leads me to regard it as an “abstraction” rather than as a proven clinical fact. Moreover, if I may judge by the “admission certificates” to the Royal Mineral Water Hospital, Bath—a fair test, as I maintain—many are of the same mind as myself, for during the past ten years I do not recall a single instance in which a patient sought admission thereto as suffering from “irregular” gout.

But some writers on gout—indeed, I think I may say all—whatever doubts they entertain as to the propriety of retaining the term, yet qualify their pronouncement in favour of some particular variety of anomalous gout, visceral, cutaneous, or other. Still, in justification of my own uncompromising attitude, I must say that dispassionate analysis of their eclectic claims, in light of present day knowledge, to my mind fails to show any adequate reason for the faith that is in them. Of some of them I feel sure that sub-consciously they have been influenced by a respect for tradition, forgetful of Pliny’s sentiment,—

But, to resume, this much at any rate may be affirmed, viz., that there is no proof that visceral disturbances or cutaneous disorders are due to uric acid. On the other hand, in view of my contention that the inherent morbid potentialities of the “gouty” demand for their fruition the intervention of an infection, the reader may rightly ask whether the same agent may not be capable of evoking the visceral or cutaneous, as opposed to the arthritic, manifestations of gout.

Trousseau, a whole-hearted advocate of irregular gout, drew an analogy between gout and syphilis. Somewhat contemptuously he observes: “To those physicians in whose eyes localisation constitutes the particular disease the differences in appearances are so many different diseases, while to those who consider that the disease consists much more in the aggregate of the general phenomena, in their evolution, in their progress (and that, thank Heaven! is the direction in which sound observation leads), these affections, differing in appearance, are only multiplied expressions of the same species of morbid action. To the real physician exostosis, alopecia, psoriasis, roseola, bubo, and chancre are always syphilis—syphilis in different garbs.” In the same way he held that the infinitely varied manifestations of irregular gout were all affiliable to one and the same morbid agent. He claimed, too, that visceral gout was “the result of a sort of imperfect inflammation analogous to that which manifests itself in the joints.”

Unfortunately for the cogency of the argument, there is no proof that such visceral inflammations as do occur in the “gouty” are of gouty origin. Unfortunately, too, the microbic agent that we postulate as responsible for “gouty” arthritis is as yet unisolated. If this disability be removed, it might be found that the said organism was capable of originating, not only the arthritic, but the alleged visceral, forms of gout. But pending such discovery I am of opinion that the term “visceral” gout should be abandoned, in other words that we should cease to talk of, e.g., bronchitis, dyspepsia, etc., as “gouty,” and should talk of them as bronchitis or dyspepsia occurring in the gouty. In this way we may escape, or, better, render uncalled for, the scathing criticism of Pye Smith:—“It has become common to ascribe bronchitis, dyspepsia, gastralgia, iritis, gravel, cystitis, and even psoriasis to the ‘gouty’ diathesis; but the evidence is very slight, and the ‘gout’ to which such evidence as there is applies is the distillation of morbid humours which belong to a bygone pathology.... There is no reason to believe that gout ever flies to the stomach, but over-indulgence at the table may produce acute dyspepsia as well as inflammation of the great toe. Elderly people are liable to gravel, gout and cough; and while lead and drink may lead to gout and chronic Bright’s disease, cirrhotic kidneys favour an attack of gout.”

Infantile Gout

While subjects of gout have told me that they had had an attack in their teens, I have never myself seen an instance. Still less can I claim to have seen what I felt justified in calling “gout” in children. On the other hand, if, as one authority states, “tonsillitis (quinsy), enlarged tonsils, granular states of the pharynx, and catarrhal conditions of the throat and respiratory mucous membranes are not infrequent expressions of gouty inheritance in children,” then, of course, all of us must be quite familiar with “infantile gout.”

But even this formidable list of legacies from gouty parents is eclipsed by a more recent writer, J. Comby (1902), who, discussing “infantile arthritism,” divides children coming of gouty stock into two types: the “lymphatic” and “nervous.” The children of the former class suffer from fleeting swelling of the lymphatic glands, rhino-pharyngitis, tonsillitis, and, if they be girls, from chlorosis. Also they are given markedly to tachycardia, bradycardia, and vasomotor ataxia. They are also especially liable to asthma and the crises of dyspnœa, and pulmonary congestion may alternate with urticarial and eczematous eruptions. Truly, their lot is hard, for they fall a ready prey to colic, constipation, all varieties of dyspepsia, not to mention nocturnal and diurnal enuresis!

Comby also claims that these gouty children are especially liable to recurrent or cyclical vomiting. In this matter he is confirmed by J. Thomson, who noted that these children not infrequently give a history of having had asthma, urticaria, eczema, stammering, and other nervous complaints, also that in many instances uric acid crystals or a copious deposit of urates have been noted in their urine.

As to the “nervous” type, they labour with insomnia, night terrors, convulsions, and when older with migraine. To these liabilities must be added undue proneness to acne, seborrhœa, psoriasis, chilblains, angio-neurotic œdema, urticaria, etc., not to mention muscular and joint aches and pains.

Whether this medley of distempers can with any pretensions to scientific reason be affiliated to a gouty heritage, or whether they can be regarded as expressions of a budding “gouty diathesis,” is, I submit, of the nature of pure speculation. That the child who suffers with cyclical vomiting may show uric acid crystals or urates in his urine is certainly no proof that he has inherited gout, much less that he is actually “gouty.” In uro-lithiasis the uric acid is precipitated in the urinary passages, viz., strictly speaking, outside the body, whereas in gout the pathological error originates within the organism. More apposite is Uffenheimer’s observation, previously noted, that children of this type suffer the same disturbances of purin metabolism as are met with in adult gouty subjects.

If the fact is confirmed that the output of exogenous purin in such children is diminished or retarded, it would certainly be a most interesting finding, possibly with a now unguessed-at significance. But we should recall that even in the subjects of regular gout such is not invariable, and, moreover, occurs in diseases other than gout. Pending further exact investigations I think it would be wiser not to indulge in such vast generalisations, mindful of the sentiments expressed by the illustrious Sydenham in his letter to Dr. Gould:—