Chapter XXIV: Irregular Gout

“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:—

(1) The subsidence or disappearance of functional visceral
derangements following the development of articular gout;

(2) Their occurrence directly after an articular paroxysm has
been apparently suppressed;

(3) Their recurrence and alternation with arthritic outbreaks,
this in some instances repeatedly;

(4) Lack of any appreciable cause for the functional
derangements and their indefinite anomalous character;

(5) Their favourable response to specific gouty therapy.

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,—

“Quamvis enim cedere auctoritati debeam, rectius
tamen arbitror, in tanta re, ratione quam auctoritate
superari.”—_Lib. i., Ep. 20._

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:—

“I have bin very careful to write nothing but what was the
product of careful observation. So when the scandall of my
person shall be layd aside in my grave it will appear that I
neither suffered myselfe to be deceived by indulging in idle
speculations nor have deceived others by obtruding anything to
them but downright matter of fact.”