TREATMENT OF GOUT
Adaptation is the keynote to progress in therapy—adaptation of our
therapeutic measures to the ceaseless advances of pathology. In
the history of gout it has ever been so, the changing, oftentimes
contradictory, vogues in treatment, always the reflex of equally mutable
and conflicting views as to its pathogeny. For who can doubt that the
facts of pathology supply the indices of rational as opposed to empirical
methods of therapy?
Albeit, much remains to be done before we can claim to fulfil the demands
of ideal treatment of gout. For we are still ignorant of its exact
etiology, cannot yet boast of our control of the morbid potentialities
that constitute the pathological groundwork of the malady. We cannot
obliterate the diathesis, and must still deplore with Sydenham that “as
for a radical cure, one altogether perfect, and one whereby the patient
might be freed from even the disposition to the disease, this lies, like
truth, at the _bottom of a well_; and so deep is it in the innermost
recesses of nature that I know not when or by whom it will be brought
forward into light of day.”
But although we cannot dissipate the inherent proclivities to the
disorder, we can, I think, claim to fulfil the humbler _rôle_, viz.,
obviate their coming to fruition. Haply in the fulness of time we may
be able to influence the _endogenous_ factors that make for gout, may
through the labours of the bio-chemist be able to translate or assess
them in terms of _functional inefficiency_ of this or that particular
viscus. But meanwhile we must perforce content ourselves with the
eradication or control of the _exogenous_ factors of gout—the _excitants_
whereby or through whose agency the malady from being _latent_ becomes
manifest and overt.
RADICAL TREATMENT OF LOCAL FOCI OF INFECTION OR TOXIC ABSORPTION
When discussing the etiology of gout we emphasised the probability of
the intrusion of an _infective_ element in its genesis. We commented,
too, on the extreme frequency with which local infective foci are
encountered in _gouty_ subjects and the imperative necessity of their
early recognition and radical treatment. In doing so, we but conform
to what should be regarded as the salient canon in the treatment of any
form of _arthritis_, viz., a diligent search for a _focus of infection_.
A _monarticular_ arthritis, such as gout in its initial outbreaks
almost invariably is, calls for the same painstaking investigation as a
polyarticular, for one never knows when the former may merge into the
latter. Nor, if we find one focus, should we rest content, assuming that
this is the only one of significance. For in many instances there are
probably several foci. Thus, how frequently are septic teeth conjoined
with tonsillar and aural troubles, and, as modern investigation shows,
these, again, may be associated with remote foci in gall bladder,
appendix, etc.
To begin with, a thorough examination of the mouth and nasopharynx
is essential. During the inspection any artificial dentures must be
removed, lest we overlook concealed and septic stumps. “Bridges,” again,
are a notable source of sepsis. The roots upon which they are fixed or
the related gums may be infected. _Phlebitis_, as we know, is a common
associate of gout, and C. A. Clark, emphasising the septic potentialities
of bridges, cites an obstinate case of phlebitis which only cleared up
after removal of a filthy device of this nature.
Again, _devitalised teeth_ that have been “crowned” should always be
suspect. Infection at the root is common, with abscess formation. Such
are not necessarily painful, and may give no indication of their presence
until they find an exit of discharge, maybe by a gumboil or _viâ_ the
antrum, etc. These abscesses around the apices of non-vital teeth are
difficult of diagnosis in their early stages. Even the X-rays may fail
to detect them when minute, this owing to the small amount of pus, or
because abstraction of the lime salts from the bone has not proceeded to
an extent that may be appreciable by skiagraphy. The first indication of
their presence is a small area of rarefaction in the bone around the apex
of the root.
It is important to recognise that teeth that appear sound upon external
examination are not necessarily so. In short, ordinary clinical
examination may be quite inadequate. Not only must the condition of the
“crowns” of the teeth, but that of their _roots_ also, be ascertained.
For when we reflect that, in addition to _abscesses_, _cysts_, _buried
roots_, _inflamed_ and _impacted molars_ may be present, we see, if we
are to achieve a full and accurate diagnosis, _radiographs of the jaws_
are essential. A single-plate negative is practically of no value. A
_series of films taken all round the mouth_ is the only satisfactory
procedure. Such give finer detail, and show up the interstices of the
teeth—the sites of predilection for _periodontal disease_ or _pyorrhœa
alveolaris_.
Passing to pyorrhœa alveolaris, which has been defined as the twentieth
century scourge, it cannot be denied that if all the evils attributed
thereto are to be nipped in the bud, then _X-ray examination_ of the
_teeth_ must be resorted to at a much earlier stage than it commonly is.
Clean as well as unclean mouths fall a prey thereto, and, as a rule,
investigation of the teeth is an after-thought, this particularly in the
subjects of _gouty arthritis_. Usually the gout has been in full swing
for years. The patient’s _dyspeptic_ symptoms have been dismissed as
“gouty,” and “alkaline stomachics,” etc., have been his lot, though his
teeth may be in a foul condition—one which would not have been tolerated
probably in any form of arthritis other than “gouty.”
But if to diagnose pyorrhœa alveolaris in its early stages we must
needs invoke radiography, on the other hand we should be careful not to
overlook its presence when advanced. The gums may be pale and shrunken,
at other times red and swollen and very prone to bleed. When pockets form
round the teeth, pus and blood may be expressed. Probing may not reveal
their true depth, whereas X-rays do.
Sometimes only one or two teeth are affected, at other times many, and
these not necessarily adjacent to each other. Thus it happens that the
disease is more advanced at one part of the mouth than at another.
Exacerbations frequently occur—a blessing in disguise. The affected teeth
become tender to bite on and loose in their sockets, but often pain
lessens, and the tooth again tightens up, and the all-necessary visit to
the dentist is again and again postponed. Sometimes abscesses form, which
discharge into the peridental pockets. Eventually the teeth may drop
out almost painlessly. Herein resides the danger of the condition, its
relative _painlessness_. Hence the ease with which _secondary infections_
may ensue, _e.g._, in the _tonsils_, the _gastrointestinal tract_, etc.,
while the original source may be altogether overlooked.
The subjects of gout are often middle-aged or old. We should recollect
then that chronic _periodontitis_ may in their instance ensue in sequence
to _senile atrophy of the alveolus_. Recently in a patient of mine nearly
eighty, a sufferer from gout and sciatica, a persistent _pyrexia_, of
apparently cryptic origin, forthwith ceased after extraction of his
teeth. He lived some considerable time afterwards, but I often regret
that his septic teeth had not been drawn long before.
Unfortunately no specific germ can as yet be saddled with the
responsibility for _pyorrhœa alveolaris_, though some would convict
the _endamœba buccalis_. _Spirillæ_ and _staphylococci_ form a
large proportion of the bacterial flora met with in _oral sepsis_,
but the results of _vaccine_ treatment would seem to indicate that
_streptococci_, _diplococci_, and _staphylococci_ are the most frequent
causes of complications. Still it must not be forgotten that the
_streptococcus viridans_ is by some held to be specially related to
_arthritis_. Hartzell (1915) invariably found it in the teeth and
peridental tissues in 220 patients suffering from arthritis. This
_streptococcus hæmolyticus_ frequently leads to _secondary tonsillar
sepsis_, and, as previously noticed, to subsequent _gall bladder
infection_, etc.
Passing to _local treatment_, if oral sepsis or pyorrhœa alveolaris
exists, carious teeth when present should be extracted, or their cavities
cleansed and filled. Accumulations of tartar should be removed, and
unhealthy gums attended to. Thus “pockets” should be swabbed, syringed,
or subjected to ionisation. Exacerbations frequently follow the
extraction of teeth. Acute paroxysms of gout have followed this simple
operation. In cases where the extraction of many teeth is called for,
it should be preceded by as thorough a cleansing of the mouth as can be
assured. It is a matter of common experience that severe exacerbations of
arthritis follow neglect of this precaution, owing to the enhanced toxic
absorption from the extensive raw surface.
Unquestionably, whether it be a matter of _curettage_, of “_pockets_,”
_alveolar abscesses_, or _extraction of teeth_, it is wiser to proceed
_gradatim_. Hartzell, when many septic foci exist in the gums and teeth,
allows three to six days to intervene between “treatments,” this in order
to gain full advantage of what may be called _surgical auto-inoculation_.
For, as he contends, any local measures, curettage, etc., necessarily
involve inoculation of the subject with a large number of organisms,
thus producing an effect similar to that of an efficient vaccine, “with
the added advantage that the constant supply is shut off from the focus
disturbed.”
Recurring attacks of _tonsillitis_—well-recognised determinants of
gouty outbreaks—demand thorough local treatment. If this fail, the
propriety of removing the tonsils will call for consideration. But,
as tonsils may be very misleading in appearance, the aid of an expert
is often indispensable. Thus the worst types of tonsillar sepsis may
exist in the small “buried” tonsil. In such cases the indications for
_enucleation_ are the more emphatic when we note the increasing evidence
that _tonsillar sepsis_ may be etiologically related to _appendicitis_ or
_cholecystitis_.
Again, as before pointed out, Wynn Wirgman noted that some cases of gout
are associated with _nasal_ disorder, and certainly in non-gouty forms
of arthritis expert treatment has reacted very beneficially on the joint
condition. Watson Williams has recently drawn attention to “_latent
sinusitis_” as a cause of _systemic infections_. He cites two cases of
chronic _rheumatoid arthritis_ which, previously resistant to treatment,
were greatly improved by operation on the _sphenoidal sinuses_. The
washings from the sinuses were free from pus, but on culture showed
growths, in the one case of _streptococcus albus_ and in the other of
_streptococcus aureus_ and _streptococcus brevis_.
Needless to say, the genito-urinary tract should be carefully
investigated, especially in polyarticular gout, or monarticular when
located in unusual articular sites, this if only to eliminate the
possibility of a latent _gonococcal_ infection. Apart from this, we
should recollect that _cystitis_ is common in gouty subjects, and,
according to older authors, might occur as a result of “_metastasis_,”
not to mention the cases of so-called “gouty” _urethritis_, which, it
is claimed, not uncommonly supervenes at the end of an articular attack
of gout. Nor should we forget the _rectum_, for hæmorrhoids are not
uncommon in these subjects. Years ago Garrod noted that the cessation of
a habitual hæmorrhoidal discharge frequently proved the signal for an
outbreak of gout. Moreover, there is increasing evidence that _rectal
ulcerations_ may be causally related to some forms of arthritis.
When all the foregoing regions have been thoroughly investigated the
lower levels of the gastro-intestinal tract must be thoroughly examined
by all modern methods. Diminution, absence, or excess of free HCL may
call for determination, while X-ray studies may afford us an explanation
of dyspeptic symptoms. Lastly, the urine and fæces may call for
exhaustive investigation.
In conclusion, however, if there be any local focus of infection so
situated as to admit of radical measures, these should be undertaken
prior to resorting to vaccine therapy.
But, obviously for the success of vaccine therapy, it is essential that
an accurate _bacteriological_ diagnosis of the case under consideration
be accomplished, which of course is comparatively easy if we are able to
isolate the particular organism by direct cultural experiment. To this
end cultures should be made from the roots of extracted teeth, the gums,
tonsils, or nasal or other discharges. Albeit, we must never be content
to select haphazard any organism that we may isolate from the patient’s
mouth, nose, urine, fæces, or elsewhere. Doubtless the true clue will
lie in the institution of _complement fixation tests_ for the organisms
responsible for local infections. Research to this end is now in course
of progress at the Royal Mineral Water Hospital, Bath, for it is becoming
increasingly clear that nothing short of “team-” work will suffice for
the full elucidation of the “gouty” and the non-gouty arthritides.
DIET
Truly in respect of diet the gouty have “suffered much of many
physicians,” have been the butt, so to speak, of all the fads and
frailties of medical opinion. Should that chemical outcast “uric acid”
but appear in excess in the urine, it was, and still is for many, an
infallible index, not only of gout, but of gout maintained and nurtured
by improper feeding. The inference seemed obvious: the ideal diet for the
gouty was a diet free from any uric acid-forming material. This achieved,
the gouty “will be free from his leprosy, and henceforward, if he abide
by the prescribed regime, all will be well with him.” But, as Sir James
Goodhart, from whom we take this last passage, pertinently asks, “is this
so?” The answer is, I fear, in the negative. For who has not met with
gouty veterans who, having run the gamut of endless dietetic experiments,
still remain “gouty,” though, _mirabile dictu_, still avid for fresh
ventures?
For myself, I know of no stereotyped diet for the “gouty,” for in this
respect every man is a law unto himself. “Get the acid out of your
system,” is the watchword of many, and, I fear, often to the undoing of
their victims. Bent on the annihilation of the disease, they overlook
the _individual_. But, weary of futile chasing of uric acid out of the
economy, most students of gout now agree that the aim of all dietetic
measures should be to secure, as far as possible, _gastro-intestinal
asepsis_. For, as experimental studies have shown, it is possible, by
means of a judiciously selected and varied diet, to modify the character
and even to inhibit the growth of the intestinal flora. The far-reaching
nature of such an influence is clear when we reflect that all abnormal
fermentative and putrefactive processes in the alimentary canal appear to
be referable to the action of microbial agents.
_Diet in Acute Paroxysms._—The initial outbreak of gout may occur at
any age, and respect must be had to this as well as to other individual
peculiarities. If the subject be young, say in the forties, and a free
liver, he may at the onset experience distaste for food, if not actual
nausea. If so, let him follow his bent, and confine himself to hot water,
barley-water, or hot weak tea. Such a modified process of starvation
is beneficial rather than harmful. Drinking freely of bland diluents
promotes the elimination of toxic or waste materials, while the intake of
hot water stimulates the hepatic cells and promotes the excretion of bile.
Milk, easy of digestion and rapid absorption by a febrile patient, is the
ideal form of nourishment. Moreover, a milk diet constitutes the most
effectual means of attaining a comparative degree of intestinal asepsis.
From two and a half to three pints may be taken in the twenty-four
hours. While some will find no difficulty in assimilating it, others
soon experience nausea, vomiting, and even diarrhœa, from the passage of
undigested curds. It is therefore advisable to begin with small amounts
given at regular intervals. If ill digested, it may be diluted with some
alkaline water, or three to five grains of citrate of soda added to each
tumblerful.
To obviate monotony the intake may be varied by oatmeal or barley gruel,
veal, mutton, chicken, or vegetable broth, but strong soups and animal
extracts must be avoided. There is no objection, however, to bread and
milk, tapioca, semolina, or sago puddings.
With the disappearance of fever and the decline of acute symptoms fish
may be introduced into the dietary, with later on a little white meat or
chicken. This may be safely done when local pain and tenderness decline,
and alike the tension of the parts, as shown by pitting. Moreover, at
this stage the appetite usually asserts itself. Still the return to
regular diet must be made slowly and cautiously, if we wish to combat the
very common tendency in these patients to functional _gastro-intestinal_
and _hepatic_ derangements. Lastly, in acute _sthenic_ gout occurring in
a robust subject there is no need whatever for _alcohol_ in the _febrile_
stage. Also, it may be added, the younger and the stronger the patient,
the better will he thrive on a pure milk or a lacto-farinaceous diet, and
the less urgent the necessity for relinquishing the same until all fear
of a relapse has passed.
On the other hand, in acute _asthenic_ gout in an _elderly_ and perhaps
somewhat _debilitated_ subject one must more than ever have regard to
the individual, especially if he be an old time sufferer, perhaps with
multiple joint involvement. Such a man “has not so much the gout as the
gout has him.” He has to be helped to support his burden. In short, the
diet for the _young_ and _plethoric_ differs from that suitable for the
_old_ and _asthenic_.
Restriction of such to a milk diet is sometimes positively harmful.
The mischief is, that, once begun, every attempt at a more varied diet
immediately provokes a relapse.[60] As Sir Thomas Watson wisely observed:
“They must be allowed a certain quantity of their accustomed good cheer,
or they become an easier prey to the disease. In such cases you must
‘trim’ as well as you can between opposite dangers, between the Scylla of
excess and the Charybdis of debility.” In short, you must maintain their
vigour and their strength. For this a pure milk diet will not suffice.
In addition thereto, pounded or minced chicken, a little fish, sole or
whiting, may be given. When also, as often happens, they have been wont
to take alcohol, two ounces of mature brandy or whisky, well diluted with
Salutaris or other mineral water, may be allowed them every twenty-four
hours.
Indeed, if the subject be old and broken down, it may be necessary to
increase the amount of stimulant. In such cases to go on treating the
_disease_, heedless of long-established habits, is bad policy. Wholly to
withhold alcohol may well precipitate disaster. Homilies on abstinence or
temperance are best postponed pending convalescence.
Moreover, these cases of _acute gouty polyarthritis_, whether in the
middle-aged or old, very commonly run an _afebrile_ course. If then,
as not infrequently happens in these distressing cases, the patient’s
progress is slow and unsatisfactory, there need be no hesitation in
renouncing a strictly lacto-farinaceous regimen in favour of a more
mixed diet: clear vegetable soups, well-made Julienne, mutton, veal, and
chicken broths, lightly boiled fish of the digestible kinds, pounded and
minced chicken, etc.
Even when in these cases _pyrexia_ is present, it is rarely continuous,
but is diversified by _afebrile_ intervals. If then, while the paroxysm
is in full flare, it be deemed advantageous to adopt a milk diet, it is
all the more important that in the _inter-paroxysmal_ stages we take full
advantage of these periods of enhanced digestive capacity.
_Diet in Chronic Gout._—Sydney Smith, writing to the Countess of Carlisle
in his seventy-first year, humorously apostrophises his gout: “What a
very singular disease it is! It seems as if the stomach fell down into
the feet. The smallest deviation from right diet is immediately punished
by limping and lameness, and the innocent ankle and blameless instep are
tortured for the vices of the nobler organs.”
Precisely so, but what constitutes the “right” diet? We are told that
this is good and that is bad for gout. Some would have us eschew red meat
and cleave unto white; for others common salt is the devil that must be
cast out. Some speak ill of all the fruits of the earth. Strawberries
especially, they say, are the bane of gout, yet in these same Linnæus
found salvation. For many, again, sugar is anathema, tea and coffee but
uric acid solutions, and alcohol in all forms rank poison!
What a trial the gouty subject who, obsessed by his “acidity,” has passed
through the furnace of many spas! “Everything I eat turns to acid” is his
plaint. He has been all things by turns—a fruitarian, a vegetarian, no
meat or all meat, etc. Such persons, in truth, are “uric acid” maniacs.
But—forget it not—they are of our making, and often in their multitude
of counsellors have found, not wisdom, but _starvation_! Well would it
be if the evil done ceased with themselves, but unfortunately they seek
converts to whatever cult they affect.
_The Fallacy of Fixed Dietaries._—As Bacon in his “Regimen of Health”
(1597) wisely observes: “Some physicians are so regular in proceeding
according to art for the disease as they respect not sufficiently
the condition of the patient.” The wisdom of this has, I fear, been
overlooked by those who hold that the ideal diet for the “gouty” is one
destitute of the _precursors of uric acid_. Its acceptance makes not for
flexibility in dieting, but rigid, undiscriminating routine.
Apart from the violation of principle, the direct result is, that the
victim runs amok among the _carbohydrates_, with as a frequent penalty
an _acute_ outbreak, this although uric acid is not a direct product of
carbohydrate metabolism; nor, as far as is known, does the carbohydrate
intake influence the rate of formation of uric acid. Thus do theory
and practice come into conflict, and, as usual, the patient pays. How
pernicious this obsession that uric acid is a morbid agent! Uric acid is
not an etiological entity, and, as Walker Hall rightly observes, “it is
high time that every practitioner made a point of fully educating the
public in this respect.”
Any attempt to formulate a set dietary proves but a snare and a
delusion. No regime is applicable to the “gouty” as a class, nor even
to the individual “gouty” subject at all periods of his life history.
His disease persists for an indefinite period, and, like most chronic
maladies, undergoes variations. _Pari passu_ his digestive capacity
rises and wanes. The regime therefore must be adapted and readapted to
his varying necessities. For it is the _patient_, and not the “gout,”
dictates the diet. But only too commonly the _disease_ is dieted, the
victim ignored—_hinc illæ lachrymæ!_
Our dietetic ventures must obviously rest on a sounder basis. This we do
know, viz., that _functional disturbances of digestion_ generally precede
a “gouty” paroxysm, and that their amelioration is followed by relief of
symptoms. The aim of our dietetic measures then is the _prevention of
digestive disturbances_, not the routine withdrawal or reduction of uric
acid precursors.
The dietetic treatment of the “gouty” is that of the “dyspeptic,” with,
if anything, an added discrimination, for an unknown factor intrudes—the
“gouty diathesis”—which has also to be reckoned with, but of this later.
Now “dyspeptics” cannot be dieted by rule of thumb. Whether they be
“gouty” or “non-gouty” matters not. A careful study of the phenomena of
digestion, if not essential in every case, is certainly called for in the
more obstinate and obscure forms. In short, an attempt should be made
to determine the special form of “indigestion.” Is the derangement of
function a disorder of motility or secretion? Is it catarrhal or nervous
in origin?
That such is the proper mode of procedure is undeniable. For are we
not too prone to assume that the “dyspepsias” of the “gouty” are _sui
generis_, all due to _one_ cause, the _materies morbi_ of _gout_, instead
of being merely “_excitants_” of gout and due to a variety of digestive
functional disabilities, and these of equally diverse origin?
_Thorough Physical Examination a Necessary Prelude to Dieting._—When we
recall that the “dyspepsias” of the “gouty” endure through long years,
the suggestion that every effort should be made to localise and establish
the exact nature of the underlying derangement seems almost superfluous.
Yet how often is the question dealt with offhand, though, ideally
speaking, I cannot help thinking that the _primary_ outbreak of _gout_
should be the signal for an exhaustive examination by all modern methods.
The consequences of dyspepsia in the “non-gouty” are bad enough, but
infinitely more so in the “gouty” subject. But it is the former group,
not the latter, that has been the favoured object of study by experts,
which is, I think, somewhat unfair.
There is need of a searching investigation, a more common invoking
of the tests whereby the functional efficiency of the stomach may be
gauged. We know that there may exist on the one hand hyperchlorhydria
and on the other hypochlorhydria. But we need to know more as to
disturbances in gastric motility, delay or hurry in digestion, not to
mention abnormalities in shape, position, size, tone, pyloric end rhythm,
etc. In view of the almost general admission that _gastro-intestinal_
derangements are causally related to outbreaks of _gouty arthritis_,
surely our remissness in this matter is somewhat surprising, the more so
in light of the heroic procedures, viz., _ileocolostomy_ and _colectomy_,
advocated in _rheumatoid arthritis_, a condition by many deemed related
to gout.
Leaving such aside, none will, I think, deny not only the value of _test
meals_ for _free HCL variations_ and experimentation with all kinds of
foodstuffs, but also of X-ray examination of the _alimentary tract_.
How subversive of all preconceptions the revelations of radiography
in _gastric_ and _intestinal_ conditions, of what infinite value in
disentangling the ambiguous significance of purely subjective sensations!
Thus, alterations in _gastric_ tone, motility, and peristalsis may hark
back to remote lesions in _gall bladder_ or _appendix_, and these also
account for variations in free HCL.
“Great eaters,” said Sydenham, “are liable to gout, and of these the
costive more especially”—an observation the truth of which all will
confirm. It may be taken as a maxim that nothing for the gouty is more
prejudicial than _constipation_. Here it is obviously of importance that
we know the site of delay, whether in the lower coils of the ileum, the
colon, or merely the rectum, _i.e._, dyschezia. How else obtain this
information, save through X-ray examination?
Any departure from normal in consistency, colour or content of the fæces
should be noted so as to identify _hepatic_ or _pancreatic_ derangements.
An analysis of the urine should always be undertaken, its reaction noted,
the presence of albumen or casts ascertained. It is important, too, that
we do not overlook _glycosuria_ or _oxaluria_, or substances indicative
of excessive intestinal putrefaction. All these bear far more pertinently
on _diet_ than estimates of _uric acid_.
The behaviour of the _skin_, whether inactive or not, must also be
taken into consideration. Moreover, as the subjects of gout are usually
middle-aged or old, it is highly important to note the general drift of
metabolism, whether in the direction of _obesity_ or undue _leanness_.
Herewith we must take an inventory, as it were, of the subject’s general
mode of living. What are his habits in respect of food and drink? Is his
diet excessive or improper in quality? Are his meals taken at irregular
times? Does he masticate his food properly?
In the matter of _exercise_, his occupation or pursuits require thought.
Do they involve excessive exertion or favour a sedentary habit? For
both these factors bear narrowly on his power or not of disposing of
ingested material. Indeed, all the foregoing reflections stand in close
relationship to the complex processes of digestion and metabolism,
and the efficacy of our prescribed regime will depend on how far our
suggested innovations meet the particular needs of the subject under
review.
_Need for Collaboration of Clinician and Bio-chemist._—Before we shall
be able to lay down a diet for the “gouty” on truly scientific grounds
much remains to be done. Our clinical examinations, in no way to be
despised, must nevertheless be supplemented by the more subtle tests of
the bio-chemist. Consider the complexity of the problem. We have to diet
not only the “gouty,” but the “potentially” gouty.
They shade the one into the other. Even the man who has had gout has
his periods of respite, of apparent unblemished health. If seen at such
a juncture, he may display the relics of his gouty attacks, _i.e._,
_tophi_. But can we say of him that he actually _now_ has gout? He has
crossed the Rubicon, disclosed his morbid trend, but meanwhile he has
apparently recrossed to the vantage ground of normal metabolism. He
stands again with those who are about to, but have not yet developed the
disorder, _i.e._, the “potentially” gouty.
Who will deny that it is when a man is, so to speak, gravid with, but not
yet delivered of, gout that dietetic measures will avail him most? But
this, alas! carries with it as its postulate the diagnosis of _latent_
gout. Now, Walker Hall suggests that “the nuclein metabolism of the
gouty patient is run at high pressure or full capacity, instead of the
usual normal quarter or at half-pressure capacity, in order to cope with
the ordinary processes of assimilation, and that there is very little
reserve energy.” Does not this seem to indicate that a fruitful sphere
of research might be the invoking of “endurance” tests and other methods
of determining the _functional capacity_ or _efficiency_ of the various
_viscera_?
At present we content ourselves with blaming the stomach, the liver, the
kidneys, etc., and often on very inadequate grounds. It would be a great
step forward if we could determine betimes which particular _viscus_ is
_functionally deficient_. There are signs that this boon will not be
long withheld, signs that not only can the functional efficiency of the
_stomach_ be tested, but also of the liver, kidneys, and even the spleen.
Thus Labbe and Daughin study the colloidal nitrogen in the urine, and
find the ratio to the total nitrogen much augmented when the _functional
efficiency of the liver is depressed_. Again, Bauer and Spiegel use
the _bilirubin content_ of the _blood_ to the same end. They maintain
that there is a bilirubin threshold, the assessment of which denotes
the _functional capacity_ of the _liver_. In health the _blood content_
thereof is surprisingly _uniform_. But in passive congestion of the
liver it rises very markedly, and the same after administration of
_cholagogues_.
In like fashion the value of _blood urea_ concentration is extolled by
Kast and Wardell as a satisfactory index of the _functional power_ of the
_kidney_. The _uric acid_ content of the blood is by Baumann, Hansmann,
Davis, and Stevens regarded as a very delicate index of _renal_ function,
though unreliable in the presence of œdema, cardiac decompensation, or
when the urine is highly concentrated in hot weather. These are but a
few of the methods available, and in the same way Frey has devised tests
for the functional efficiency of the _spleen_, while Barton invokes the
administration of urea, chlorides, adrenalin, creatine, etc., to assess
the functional capacity of the _liver_, _kidney_ or _spleen_.
Such is the trend of modern medicine—to link up clinical with laboratory
findings—and in gout perhaps more than in any other disease is this
collaboration urgently called for. For who can doubt that gout is a
malady of mixed intrinsic (endogenetic) and extrinsic (ectogenetic)
origin?
We need to know more about the _endogenous_ factor, the basal perversion
of cell structure or function, that differentiates the tissues of
the “gouty” from those of their fellows. For it is these inherent
peculiarities—structural, physical, or chemical—that give to the disease
its _sui generis_ character. How then in the “living” subject shall
these hidden morbid potentialities be identified? How save through the
medium of _function_, the outward expression of metabolic activities, in
other words by appraisement of the _functional capacity_ of the various
_viscera_? For gout primarily is a disorder of function, or, as Rendu
phrased it, a primordial “vice of nutrition.” Hence our insistence on
the invoking of the various laboratory methods for elucidating the
_functional_ powers, the efficiency or not of the _liver_, _kidneys_, etc.
This satisfactorily achieved, we may, through their reflected functional
disability or disabilities, divine somewhat the nature of the innate
tissue peculiarities of the “gouty,” may hope at long last to translate
the misty “gouty diathesis” in terms of _functional deficiency_,
deficiency of the working capacities of the _stomach_, _liver_, or
_kidneys_, and perhaps find that the basal flaw in some lies in the
_liver_, in others in the _kidney_, and thus the older clinicians be
justified of their claims for “hepatic” or “renal” varieties of gout.
That _exogenous_ factors, _i.e._, _infections_, bring to fruition these
latent morbid tissue potentialities of the gouty, is my belief. Hence
my contention that dietaries for the “gouty” should be such as promote
_gastro-intestinal asepsis_. Albeit, _infections_ are but the “seeds,”
and who can doubt that the ideal diet for the “gouty” should also take
cognisance of the “soil”—the pathological groundwork of gout?
The “soil” in gout is, I believe, one peculiarly favourable to microbic
invasion, and here again recent studies of the _cytology_ of the
blood bid fair to yield us some criterion whereby the “degree of body
resistance” to infections may be gauged.
But until the bio-chemist reveals to us the why and the wherefore of
their peculiar tissue vulnerability our dieting of the “gouty” must
perforce consist largely in diminishing the _exogenous_ excitants of the
malady. Ultimately, when researches now in progress have fructified,
we may be able to influence the _endogenous_ factors, may correct
the functional defect of this or that viscus, stabilise the nuclein
exchanges, and heighten the resistance of the tissues. In short, as Sir
Archibald Garrod puts it, “we must consider the soil as well as the seed
which falls upon it, and that he is the best exponent of the healing art
who treats the individual patient rather than his disease.”
“_The Accessory Food Factors._”—“Due nourishment, not gluttonous
delight,” is the true clue to the rational dietetic treatment of the
“gouty.” But this question of “due nourishment,” how complex it grows
in light of recent revelations. Thus, it is now generally agreed that
to satisfy the animal needs for growth and the maintenance of nutrition
something more than a due admixture of proteins, fats, carbohydrates, and
inorganic salts is essential.
We must, of course, ensure that the caloric value of the food intake be
adequate, and the supply of protein sufficient to maintain the nitrogen
balance, also that the intake of protein suffice for the exigencies of
tissue waste, not forgetting that for this is required a sufficient quota
of the individual primary fractions of the protein molecule.
But this, we now know, is not all, for there are other and indispensable
dietetic components. In the food we eat are substances of hitherto
unguessed-at potency—the “vitamines,” or, as they are now more properly
termed, “accessory factors of diet.”
Of these elusive bodies but three as yet have been isolated: _fat-soluble
A_, _water-soluble B_, and _water-soluble C_. In infancy absence of the
first-named “vitamine” leads to _rickets_. Lack of the second engenders
_scurvy_, of the third _beri-beri_.
But, apart from these well-defined “deficiency diseases,” McCarrison
has pointed out that the absence of these “accessory food factors”
leads to grave _functional_ derangements, especially of the organs of
digestion and assimilation and those subserving endocrine functions,
not to mention malnutrition of the nervous system and the induction of
hyperadrenalinæmia and chronic inanition.
A heavy indictment, but, more pertinently to our subject, McCarrison
inclines to think that _bilious vomiting_, _cyclical acidosis_, _mucous
disease_, and other _metabolic_ disorders met with in _children_ are very
probably due to deficiency of certain “accessory food factors.” In light
of this it is interesting to recall that these same symptom complexes are
by Comby and others regarded as manifestations of _infantile gout_.
More arresting still is McCarrison’s observation that all the clinical
phenomena distinctive of “deficiency diseases” as a whole are apparently
the result of _nuclear_ starvation of all tissue cells. In short, these
“accessory food factors” are essential to _due nutrition of the nuclear
substance_. How interesting this in light of the generally accepted
view that “gouty” individuals are victimised by some inherent defect or
alteration of _nuclein_ metabolism. Does not this seem to indicate that
one of the clues to successful dieting of the “gouty” must be adaptation
of the nuclein intake to the needs of the individual, in short that
we must strive for the stable maintenance or conservation of nuclein
metabolism?
Again, as before stated, one of the results attaching to deficiency
of “vitamines” is _functional derangement of the organs of digestion
and assimilation_. Such disturbances are prominent in _gout_, and that
“errors of diet” play an important _rôle_ in the genesis of the disorder
can scarcely be denied. At the same time there is no proof as yet
that the absence of some mysterious “accessory factor” makes for the
development of the disorder.
Nevertheless reflection on these findings is, I think, wholly apposite.
It should, at any rate, chasten those who affect extreme dietaries on
insufficient grounds. They are not justified of results, for, with Sir
Archibald Garrod, I venture to doubt “whether by dieting our ‘gouty’
patients we achieve nearly as much as we think we do.”
Such good, moreover, as we do compass, is, I think, exerted _indirectly_.
Even in the _inter-paroxysmal_ periods of the disorder, despite good or
perhaps exuberant health, gout is there. Its morbid tissue potentialities
are _latent_, though _functionally inactive_. To maintain this state of
_passivity_ is the aim of all dietetic measures, viz., to diminish or
withdraw the dietetic factors that are _provocative_ of gout.
The diet most void of offence is one the least calculated to excite
_digestive disturbance_—one that makes more surely for _gastro-intestinal
asepsis_. At this juncture it is interesting to note McCarrison’s
observation that although the absence of certain “accessory food factors”
is the essential etiological agent in the genesis of “deficiency
diseases,” yet he holds that _infections_ and parasitic agencies are
often important causes in determining the _onset of symptoms_.
Similarly in the causation of gout, “errors of diet” are not the only
agencies at work. They are in truth but contributory factors in that
such indiscretions favour the incidence of catarrhal states. These again
promote increased toxicity of the intestinal flora with sequential
disturbance of general _nuclein_ metabolism and associated specific local
reactions in certain tissues.
I make no apology for this somewhat lengthy digression. In the sphere of
dietetics, as elsewhere, “a little knowledge is a dangerous thing.” We
need to walk more circumspectly in this matter of dieting; and to this
end reflection on the disabilities that still beset us cannot fail to be
salutary, and will form, I think, a fitting prelude to our suggested mode
of procedure.