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.”